Cells, Ketosis and Aging

Today, Dr. Mike Eades has a fascinating article on his ProteinPower Blog, Ketosis cleans our cells.

It’s one of those “must read” items of the day – so without further ado, go…go read it!

Low-Fat May Increase Relative Risk for Cardiovascular Events

Back in 2003, researchers decided to see how good the DASH Diet is compared to the Standard American Diet. They designed a twelve-week trial with a two-week run-in where the diet over those two weeks contained 37% total fat with 16% of calories from saturated fat. With 100 subjects participating, 50 were randomized to consume the DASH Diet while the other 50 were on their own to eat as they wished – this second group was the “control group.”

This particular study was well-designed – it not only sought to investigate the impact of diet on cholesterol levels, but also C-Reactive Protein (CRP), a marker of inflammation in the body that we understand is a pretty good predictor of cardiovascular risk – more so than cholesterol levels.The DASH Diet really modified what the intervention group ate. Their diet contained just 27% total fat and just 6% saturated fat.

So, what happened after three months on this “better” diet?

Not much in the way of benefit. In fact, some findings were downright scary and the conclusions in the abstract only hint at how poorly some on the DASH Diet fared compared to the control group, “the presence of increased CRP was associated with less total and LDL cholesterol reduction and a greater increase in triglycerides from a reduced-fat/low-cholesterol diet. These findings document an additional mechanism by which inflammation might increase cardiovascular disease risk.”

Notice, the researchers don’t say anything in their conclusions about how we might need to re-think our dietary recommendations, especially in those with elevated CRP levels? How about I show you what happened, what the data actually tells us?

First, here is the full-text of the article Inflammation modifies the effects of a reduced-fat low-cholesterol diet on lipids: results from the DASH-sodium trial.

Those placed on the DASH Diet had median baseline cholesterol levels

Total Cholesterol = 204.3
LDL Cholesterol = 131
HDL Cholesterol = 48.7
Triglycerides = 89.48
TC/HDL Ratio = 4.2LDL/HDL Ratio = 2.6

When the group was divided into those who had a baseline CRP below or above the median the results were indicative of how damaging a low-fat diet can be:

For those with CRP below the median CRP of 2.37 the following happened:

Total Cholesterol = 176.47
LDL Cholesterol = 110.29
HDL Cholesterol = 45.66
Triglycerides = 90.37
TC/HDL Ratio = 3.86
LDL/HDL Ratio = 2.4

No one can argue – they did pretty good. Not blow your socks off impressive, but they didn’t get appear to get worse and their TC/HDL and LDL/HDL Ratios did improve slightly. Keep in mind though, the diet did nothing to reduce their level of CRP though. We’ll get to that in a moment. For now, let’s see how those with CRP levels above the median fared…

Total Cholesterol = 201.63
LDL Cholesterol = 130.03
HDL Cholesterol = 46.44
Triglycerides = 110.75
TC/HDL Ratio = 4.34
LDL/HDL Ratio = 2.8

This “unfavorable outcome” on these subjects’ health occured in just three months and the best the researchers could do is bury it in the full-text rather than make it very clear in their abstract that the difference isn’t just the minor inconvenience of “less total and LDL cholesterol reduction and a greater increase in triglycerides from a reduced-fat/low-cholesterol diet” but statistically significant differences that had real potential to negatively impact health if such changes continued with eating such a diet over the long-term.

Not only did the diet result in an “unfavorable outcome” for these individuals, but when it did not change their CRP level that means that this change increased their relative risk for a cardiovascular event – basically increased their risk to have a heart attack.

Let’s explore why the CRP levels were important here – not just for those with above the median levels, but also those below the median. First, the researchers interpretation that those with CRP below the group median had a favorable outcome with the diet is misleading in my opinion. While the diet did have an effect on cholesterol levels and ratios, it had NO EFFECT on the CRP levels of the subjects following the DASH Diet.

The abstract states this “The DASH diet, net of control, had no effect on CRP.”

If we use Ridker et al’s assessment of risk, developed in the New England Journal of Medicine publication of Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events, we find that the baseline risk of those assigned the DASH Diet was a relative risk of 2.9. That is, when they started the DASH Diet they already had a 2.9 times greater risk of a cardiovascular event than someone with a “normal” CRP value of 1.6 or less. Let me be clear here – 1.6 may even be considered high if we use the Framingham data as a benchmark, but for now, let’s stick with the Ridker et al method to assess risk.

Because their CRP didn’t change, even the change in their cholesterol and TC/HDL didn’t improve their relative risk. It actually made it worse! We must consider that the diet did not change their CRP level when determining risk here and use the value they used – 2.37. In Ridker et al’s assessment protocol, that level combined with a TC/HDL ratio of 3.86 translates to a relative risk of 3.5 times greater risk of a cardiovascular event than someone with a “normal” CRP value of 1.6 or less. Did you catch that? The relative risk increased from 2.9 to 3.5!

For those who had a CRP above the median, we again must maintain no change in CRP from baseline as the data suggests. Here, the change in risk is dramatic because the TC/HDL Ratio changed so much. For those eating the DASH Diet who had a CRP above the median, the resultant change in their TC/HDL Ratio increased their relative risk to a 4.2 times greater risk of a cardiovascular event than someone with a “normal” CRP of 1.6 or less. Their relative risk increased from 2.9 to 4.2!

Let me be clear here – Ridker et al published their work almost a year before this DASH Diet trial – yet the researchers didn’t even consider discussing the implications of the findings in terms of relative risk. Instead they couched their words with phrases like “less favorable” and “likely relationship” between diet and lipids without any real fear the DASH Diet might not just cause an “unfavorable” outcome in terms of lipid values (cholesterol readings) but real world problems, like an increased relative risk for cardiovascular events!

Ridker et al aren’t the only ones to find such a disturbing relationship with CRP and relative risk either!

In October 2001, the International Journal of Obesity and Related Metabolic Disorders published findings from Pannacciulli et al, C-reactive protein is independently associated with total body fat, central fat, and insulin resistance in adult women. Their findings – Our study has shown an independent relationship of central fat accumulation and insulin resistance with CRP plasma levels, thus suggesting that mild, chronic inflammation may be a further component of the metabolic syndrome and a mediator of the atherogenic profile of this syndrome. [I chose this particular study as an example because those who followed the DASH Diet had a mean BMI of 29.3 – they were bordering on obese and had elevated CRP levels!]

In June 2001, the journal Atherosclerosis, published The association of c-reactive protein, serum amyloid a and fibrinogen with prevalent coronary heart disease–baseline findings of the PAIS project, which concluded that “CRP, SAA and fibrinogen, which are markers of inflammation, were positively and significantly associated with prevalent CHD.”

So the concept that CRP is a valuable marker and when measured should be used as part of an assessment of risk isn’t really a stretch here. The researchers failed to acknowledge its potential importance, the increased relative risk even in those with CRP below their baseline measure and especially in those with CRP above their baseline measure. Their simple conclusion that some realize less benefit from the DASH diet totally fails to recognize that neither group reduced their relative risk for a cardiovascular event – in fact, both groups had an increased risk after three months – one group moreso than the other – but both still increased their risk!

And now, some three years later, with even more trials completed, even more data showing the same miserable effects, we’re still being told that DASH and other low fat dietary approaches are better for us!

Better than what? Perhaps better at increasing relative risk?

The data shows they’re no better or worse than the Standard American Diet – which I’m sure you’ll agree is certainly not leading us to better health and quality of life long-term. So then, what exactly is a low-fat diet better than since almost every trial is comparing it to the Standard American Diet? I know I’d like to know.

We’re told it’s better, but for some reason no one can tell what it’s better than – and don’t forget we’re not told about the risks to many of us from these “better” diets – risks that are clear as day when you look at the data and not just rely on the basic information in the abstract! Not a peep from the AHA about this finding or any caution about how this dietary approach – DASH – may really negatively affect someone with a high CRP level.

Don’t you think it’s time we took this stuff seriously and actually looked for a dietary approach that works as promised – ya know, one that does optimize health and well-being over the long-term, that does reduce the risk of disease and premature death and that is based on evidence instead of prevailing dogma?

Of Mice and Men

An interesting study was published in the Proceedings of the National Academy of Sciences from researchers at Oregon Health & Science University who discovered that removing a gene involved in repairing damaged DNA causes mice to develop the metabolic syndrome.

The findings were the subject of the article, Removing DNA Repair Gene Causes Metabolic Syndrome, published in Genomics and Proteomics last week.

Those of you who are frequent readers of my column know I am cautious about trying to extrapolate findings from animal models to make a case for why things happen in humans. This finding however, is fascinating. Indeed, it may open the door to truly understanding what is happening in the metabolism of a person developing and eventually presenting with metabolic syndrome – characterized by the following features: obesity, hypertension, dislipidemia (high LDL and triglycerides with low HDL), insulin resistance and high blood sugars.

This study is the first to link DNA repair with the metabolic syndrome, and the findings suggest an important role for what is the “NEIL1 gene product” in the prevention of the diseases associated with the disorder, including obesity, hypertension, high cholesterol, insulin resistance and kidney disease. R. Stephen Lloyd, PhD, senior scientist at OHSU’s Center for Research on Occupational and Environmental Toxicology (CROET) and co-author of the study said that “…if there are catalytically compromised forms of NEIL1 within the U.S. population, these people will be predicted to be at increased risk for developing the metabolic syndrome,” a disease believed to affect more than 40 million Americans. Lloyd and his colleagues originally discovered the NEIL1-deficient mouse’s propensity for developing the metabolic disorder about two years ago.

Where this gets really interesting is in the explanation of what happens when this piece of DNA is lacking or damaged.

“If you have oxidative stress inside the cell, then the bases in the DNA can become damaged, and the responsibility of this whole group of enzymes is essentially to monitor the entire genome, looking for genomic bases that have been oxidatively damaged,” Lloyd explained. “They have the responsibility of then removing the damaged bases, which initiates a process by which the cell puts in a normal piece of DNA where the damaged DNA was. This happens every second of your life.”

Llyod and his colleague, the study’s lead author, Vladimir Vartanian, PhD, created “knock-out” mice – animals bred to lack the NEIL1 gene. Hold on to your hat – here is where the rubber meets the road of this finding – the researchers found that “the mice lacking the enzyme reached weights of between 45 and 52 grams at age 7 months, while normal mice weighed in at only 28 grams. They also were extremely lethargic, their hair was turning gray, and some were even going bald. And there were gender differences.” The male mice had more severe presentation of the features of Metabolic Syndrome, at an earlier age, than the female mice did.

“This means mutations in the NEIL1 gene, or the gene’s absence altogether, could have a catastrophic effect on the body’s ability to restore DNA to its undamaged state.”

“Our analysis is that the inability to repair damage to the genetic material, whether it is in the nucleus or whether it’s in the mitochondria, is what’s leading to a destabilization of a normal metabolic process,” Lloyd said. “That then begins to cascade and ultimately results in the symptoms that are consistent with the metabolic syndrome.”

Those last two quotes from the article are critical to our understanding of just how devastating damage to our DNA is. And, while the researchers are eager to continue with research into this particular gene to figure out how to develop a screening test for humans, I think there is enough solid understanding about what potentially damages our DNA and how to try to prevent or reverse such damage.

We must eat foods rich in nutrients – those that provide us with a full range of antioxidants – and ensure we’re eating adequate protein for our essential amino acids, along with quality fats and oils for our essential fatty acid requirements and requirement for fat soluable vitamins. While the above study was indeed only mice – the finding that a piece of the DNA missing or damaged has such a profound effect metabolically, that is it causes Metabolic Syndrome, should be setting off alarms bells in the research community!

Later today, I’m even going to show you that researchers have had warning bells going off for years in their data but have ignored it as they continue to desperately prove a low-fat diet is optimal for health. This while more and more people are presenting with Metabolic Syndrome, Insulin Resistance and Diabetes!

Anthony Colpo – Why the Low-Fat Diet is Stupid and Potentially Dangerous

For years Anthony Colpo has maintained The Omnivore, a website bursting at the seams with articles and insights into studies and claims about being healthy – all with references to studies.

This week, Colpo penned “Why the Low-Fat Diet is Stupid and Potentially Dangerous” – a lengthy and well referenced article about the null findings from the Women’s Health Initiative Dietary Modification Trial.

Today, it’s featured here, in its entirety with permission to reprint. Colpo has an amusing disclaimer at the end – you’ll probably want to read it before sending him an email if you want to communicate with him!

Why the Low-Fat Diet is Stupid and Potentially Dangerous

Anthony Colpo, February 23, 2006

On February 8, 2006, the Journal of the American Medical Association delivered a huge blow to advocates of low-fat ‘nutrition’ by publishing the results of the huge Women’s Health Initiative trial. The results of the trial clearly showed that a low-fat diet failed to prevent cardiovascular disease or cancer in women even when followed continuously for eight years. In women with pre-existing CVD, the low-fat diet increased the risk of CVD by 26 percent!

Since the publication of the WHI results, low-fat diet supporters have been working overtime manufacturing excuses for the failure of their beloved regimen. Foremost among these is that the women in the low-fat group did not reduce their fat intake sufficiently. I even had one sadly misguided soul write to me the other day telling me I did not “understand” low-fat diets, that the only reason they frequently fail is because people following them don’t lower their fat intake enough.

Such stupidity makes my head spin…

First of all, I understand low-fat diets only too well! Much to my regret, I followed one throughout most of the nineties, and the result was nothing short of disastrous.

My low-fat nightmare began in my early twenties, after a doctor told me that my cholesterol, at 213, was “moderately high” and placed me at increased risk of heart disease (something I now know to be nonsense). Following the prevailing dietary wisdom at the time, I soon adopted a low-fat diet. This wasn’t your average low-fat diet–it was a VERY low-fat diet, with the kind of anemic fat intake that would have made lipid-phobes like Ornish and Pritikin proud.

For years, I ate only the leanest meats; in fact, to this day, the thought of eating another skinless chicken breast, kangaroo steak, or low-fat fish makes me want to puke! Fuelling the high energy demands of my daily workouts in the face of a low fat intake meant eating carbohydrates–lots of them! In keeping with the common advice still given to athletes to eat lots of ‘healthy’ complex carbohydrate foods, I consumed copious amounts of rye bread, brown rice, sweet potato, wholemeal pasta, rolled oats, buckwheat, and millet.

My dedication to the low-fat mantra was nothing short of religious, and my low-fat brainwashing so thorough that when I sat down and calculated the average amount of fat calories I was taking in, I was actually proud when I realized I was consistently consuming less than ten percent of my calories as fat every day!

Halfway through the nineties, reality began to bite–hard. Despite my ‘healthy’ diet, and my daily strenuous training regimen, my blood pressure had risen from 110/65, a reading characteristic of highly-conditioned athletes, to an elevated 130/90. I noticed it was becoming increasingly harder to maintain the lean, “ripped”, vascular look that I had always prided myself on. Instead, my physique was becoming increasingly smooth and bloated. My digestive system became progressively more sluggish, my stomach often feeling heavy and distended after meals. I frequently felt tired after meals. I showed signs of leaky gut syndrome, racking up a rather impressive list of irreversible food sensitivities. I had never been much of a coffee drinker, but I was now frequently trying to fight off increasing fatigue by sipping a strong black or two before training sessions. My fasting blood glucose level was below the normal range, indicative of reactive hypoglycemia.

Basically, I felt like crap!

It wasn’t until I abandoned the whole low-fat charade, and adopted a diet that went against everything preached by the reigning diet orthodoxy, that I began to reverse these symptoms. When I ate more saturated fat and meat than ever before and subsequently felt better than ever before, I quickly realized that most diet ‘experts’ actually had no clue what they were talking about. I quickly realized that they were mere parrots repeating an official party line.
When I look back on my fat-fearing days, where I really believed that dietary fat was some sort of heinous toxin, the first thought that comes to mind is “What a wanker!” I then think of the sad legion of brainwashed folks all around the world who still follow the idiotic low-fat paradigm. “Poor folks,” I think to myself, “they really have no idea just how badly they’ve been had…”
While I feel sorry for many of these folks, I have nothing but utter contempt for those who write me in defense of the low-fat paradigm. To be fooled is one thing, but to vigorously defend those who have mercilessly deceived and shafted you is beyond pitiful–such self-destructive stupidity is an absolutely repugnant thing to observe!

Let’s now find out why the participants in the diet group of the WHI trial should be glad that they did not lower their fat intake any more than what they did!

Why the Low-Fat Diet is a Big Fat Fraud

One of the first priorities of healthy eating is to consume the most nutrient-dense foods possible. Cutting your fat intake strongly impedes this goal via at least three mechanisms:
1) Directly slashing your intake of important vitamins and fatty acids;2) Reducing the absorption of crucial fat-soluble vitamins;3) Decreasing the absorption of important minerals.
You probably think you’re being “enlightened” when you trim the fat from your meats and ditch your egg yolks down the sink. What you are really doing is lucidly demonstrating what a mindless, brainwashed dolt you’ve become. You are effectively throwing away nutrients that your body needs to survive and thrive!

The fatty portions of meat, dairy and eggs are where one finds the highest concentrations of fat-soluble vitamins such as A, D, E and beta-carotene. Stripping the skin from your chicken breast not only makes it less tasty, but reduces its vitamin A content by seventy-eight percent!(1)
Throwing away your egg yolks is equally dumb. While one large egg yolk contains 245 IU of vitamin A, 18 IU of vitamin D, and 186 mcg of lutein plus zeaxanthin, along with small amounts of other carotenoids and vitamin E, a large egg white contains none of these nutrients. Egg yolks, along with beef liver, are also an especially concentrated dietary source of phosphatidylcholine (lecithin) and choline, which the body requires for healthy liver function and for the formation of the key neurotransmitter acetylcholine. Lower levels of acetylcholine are associated with memory loss and cognitive decline(2).

The last time you chose skim milk yogurt instead of the whole milk variety, you nutritionally short-changed yourself; skim yogurt contains 93 percent less vitamin A than whole yogurt! And if you chose non-fat yogurt, then congratulations–you received no vitamin A whatsoever!(1)
Data from national nutrition surveys consistently show that American children have lower than recommended intakes of vitamin E, and this is reflected in below-average serum levels of the vitamin. Reduction in dietary fat further exacerbates the low vitamin E status of children(3). The consequences of low dietary vitamin E intakes may include impaired immune responses, and an increased susceptibility to cardiovascular disease and cancer.

Willingly reducing your consumption of important vitamins and carotenes is not smart–it’s downright stupid!

Absorb This!

Low-fat eating doesn’t just decrease your intake of certain crucial nutrients. As researchers have shown time and time again, it will also dramatically reduce the absorption of whatever fat-soluble vitamins and carotenes remain in your diet!(4-7).

When subjects ingested equal amounts of lutein–a carotenoid that may protect against age-related macular degeneration and cataract–from either whole eggs, spinach or supplements, it was observed that lutein absorption was significantly higher during the period of whole egg consumption(8).

In another study, researchers compared the absorption of carotenoids from salads that contained either 0, 6 or 28 grams of canola oil. There was no increase in blood carotenoid concentrations after the fat-free salad, while the reduced fat salad produced markedly lower blood carotenoid elevations than the high fat version(9).

The addition of 150 grams of fat-rich avocado to salsa enhanced lycopene and beta-carotene absorption by 4.4 and 2.6-fold, respectively, compared to avocado-free salsa. In the same subjects, adding either twenty-four grams of avocado oil or 150 grams avocado to salad greatly enhanced alpha-carotene, beta -carotene and lutein absorption by 7.2, 15.3 and 5.1 times, respectively, compared with avocado-free salad!(10)

Only a true dumbass would think that reducing absorption of healthful fat-soluble nutrients is somehow beneficial. Don’t be a dumbass.

Making a Bad Situation Worse

The mineral status of the typical Westerner is atrocious. Take magnesium for example, a substance vital for healthy heart function, blood sugar control, bone formation, and muscular contraction(11-16). A recent survey of U.S. adults found that the average daily intake of magnesium among Caucasian men is only 352 milligrams, and a mere 278 milligrams among African American men. Caucasian women consume an average of 256 milligrams per day, while African American women take in only 202 milligrams daily(17). The lower amounts of magnesium ingested by African Americans have been posited as a possible contributor to their increased susceptibility of hypertension, diabetes, and cardiovascular disease(18).

The situation isn’t much better for zinc. Overt zinc deficiencies are common to Third World countries where animal protein consumption is low, while milder, ‘sub-clinical’ zinc deficiencies appear to be common in modernized nations. Nationwide food consumption surveys by the USDA have found that the average intake of zinc for males and females of all ages is below the recommended daily allowance (RDA). This is especially worrying when one considers that RDAs are generally based on the amount of a nutrient required to prevent obvious, well-recognized deficiency diseases (such as stunted growth and hypogonadism in the case of zinc), not sub-clinical deficiencies that may damage one’s health over the longer-term.

Those who follow low fat diets are at even greater risk of zinc deficiency(19,20). Not only do low-fat diets discourage the consumption of zinc-rich foods like red meat, but a low dietary fat intake itself acts to impair mineral absorption.

It’s ironic that red meat is typically denigrated for its saturated fat content, because saturates are the very fats that improve mineral absorption!(21-24).

A pilot study by researchers at the USDA Grand Forks Human Nutrition Research Center examined the effect of different fats and carbohydrate on performance and mineral metabolism in three male endurance cyclists. During alternating four-week periods, each subject consumed diets in which either carbohydrate, polyunsaturated, or saturated fat contributed about fifty percent of daily energy intake. Endurance capacity decreased with the polyunsaturated fat diet. The polyunsaturated diet also resulted in increased excretion of zinc and iron, while copper retention tended to be positive only on the saturated fat diet(25).

Optimal health is next to impossible to achieve with sub-optimal mineral status. Low-fat diets, most notably those low in saturated fats, encourage sub-optimal mineral status. Yet another reason why these diets suck the salsiccia, big time!

Low-Fat, Low Omega-3

Unless you’ve been living on a distant planet for the last few years, then you have no doubt heard about omega-3 fats and their pivotal role in maintaining good health.

Unlike low-fat diets, clinical trials utilizing the sole intervention of increased fatty fish or fish oil intake have produced significant reductions in CHD and overall mortality. The benefits of EPA and DHA-rich items like fish and fish oil are not confined to the cardiovascular system. In epidemiological studies and animal experiments, increased intakes of long-chain omega-3 fatty acids have been associated with lower rates of cancer, depression and mental illness, adverse pregnancy outcomes, infectious disease, osteoporosis, lung disease, menstrual pain, cognitive decline in the elderly, eye damage, childhood asthma and attention-deficit hyperactivity disorder(26-51). In clinical trials with human subjects, researchers have observed benefits from long-chain omega-3 supplementation in the treatment of asthma, alzheimers, rheumatoid arthritis, depression, schizophrenia, infant health, pregnancy outcomes, kidney disease, menstrual problems, ulcerative colitis, Crohn’s disease and cystic fibrosis(52-73). Hell, even the fat-hating vegetarian Dean Ornish recommends the use of distinctly non-vegetarian fish oil supplements! (Gee, can anyone see a contradiction there?)

So what has this all got to do with low-fat eating? Everything!

Similar to fat-soluble vitamins, the absorption of EPA and DHA increases when consumed with a high fat meal(74).

Again, not just any old fat will do when it comes to improving one’s omega-3 status. Saturated fat improves the body’s conversion of plant-source omega-3 fats into the longer-chain varieties EPA and DHA, while omega-6-rich fats impede the conversion process. In young males, elongation of alpha-linolenic acid (ALA) and linoleic acid (LA) to DHA, EPA and AA was reduced by forty to fifty percent when dietary LA intake increased from fifteen to thirty grams per day(75).

When rats were supplemented with linseed oil, their serum and tissue content of the all-important omega-3 fatty acids increased, and omega-6 levels decreased, to a far greater extent on a saturated fat-rich (beef fat) diet than on a linoleic acid-rich (safflower oil) diet(76).
Cutting fat–as in saturated fat–worsens your omega-3 status. If you think that’s a good thing, then low-fat nutrition has already scrambled your brain. My advice: Eat some fat before you become totally brain dead!

Speaking of scrambled brains…

Nature’s Anti-Depressant: Fat!

Feeling moody? Irritable? Always snapping at your kids for no good reason? Are you known around the office as “Attila the Grump”? If so, eating a low-fat diet isn’t going to help the situation. In fact, a low-fat diet may actually be the cause of your mental funk!
In 1998, U.K. researchers reported the results of an important experiment involving twenty healthy male and female volunteers. One group was placed on a 41% fat diet, while the other group consumed a 25% fat diet. After 4 weeks had passed, the groups were swapped around so that those originally on the low-fat diet were now consuming the high-fat diet, and vice-versa. Throughout the study, all meals were prepared by the university conducting the study and supplied to the participants. Both diets were specially designed to be as palatable and similar in taste as possible.

At the beginning and end of each diet period, every subject underwent a battery of psychological assessments, including various mood state questionnaires and an interview by a psychiatrist who was blinded to the participant’s dietary status.

The study was tightly-controlled and adherence to the diets appears to have been high. HDL cholesterol levels declined during the low-fat period, a typical response on low-fat, high-carb diets, indicating that subjects ate the foods as supplied.

The researchers found that, while ratings of anger-hostility slightly declined during the high-fat diet period, they significantly increased during the low-fat, high-carb diet period!

Tension-anxiety ratings declined during the high-fat period, but did not change during the four weeks of low-fat, high-carb eating.

Ratings of depression declined slightly during the high-fat period, but increased during the low-fat, high-carb period, mainly due to two of the low-fat subjects reporting significantly greater depression-dejection ratings.

What is particularly alarming about this study is that the low-fat diet produced these symptoms in mentally healthy subjects. As the researchers emphasized, the participants were “a psychologically robust group who had never previously suffered from depression or anxiety, and who were not going through any ‘stressful’ events during the study.” They further stated that “The alterations in mood observed in the present study may have been greater if subjects were feeling more stressed or were more susceptible to mental illness.”(77)

Low-fat diets should be approached with extreme caution by those with a history of depression, anxiety, overly aggressive behavior or mental illness. Such individuals may be especially vulnerable to the nutritional inadequacies of low-fat diets.

The UK researchers’ observations raise some interesting questions. Could the low-fat, high-carbohydrate diets that have been so heavily promoted over the last thirty years be at least partially responsible for increases in anti-social behavior witnessed during the same period? If studies with our primate cousins are anything to go by, the answer to this question could well be affirmative.

Low-Fat Diet Makes Monkeys Go Ape

For almost 2 years, adult male monkeys were fed a “luxury” diet – (43% calories from fat, 0.34 mg cholesterol/Calorie of diet) or a “prudent” diet (30% calories from fat, 0.05 mg cholesterol/Calorie of diet).

Researchers observed that the low-fat diet monkeys were more irritable and initiated more aggression than the “luxury” diet animals.

The prudent diet resulted in lower total serum cholesterol levels, something that our absent-minded health authorities automatically assume is a good thing. The researchers, however, noted: “These results are consistent with studies linking relatively low serum cholesterol concentrations to violent or antisocial behavior in psychiatric and criminal populations and could be relevant to understanding the significant increase in violence-related mortality observed among people assigned to cholesterol-lowering treatment in clinical trials.”(78)

A research monkey after discovering he was going to be placed on a low-fat diet for almost 2 years.

Fatless Shrugged

It was Ayn Rand who once said that the most noble and productive goal for a person to engage in was the pursuit of their own happiness. If the achievement of your own happiness is important to you, then kick the low-fat diet’s sad, sorry, melancholy butt right out of your life–it’s a loser.

Low-Fat Diets Lower Testosterone

Testosterone is abhorred by politically correct weenies, who like to blame it for every instance of disagreeable male behavior, in much the same way menstruation was once cited as the catch-all explanation for uncharacteristically aggressive or irritable female behavior.

Of course, scientific reality is of little concern to the politically correct. The fact is, testosterone is an extremely important hormone for both men and women. Sex drive, muscle and bone health, immune function, cognitive function, mood, and cardiovascular health are all negatively affected by declining levels of testosterone. Testosterone levels typically decline with age, and, along with the decline of other key hormones, falling T levels are believed to be a major contributor to many of the deleterious changes seen during the aging process. As such, aging individuals should be looking at ways to preserve and even boost their testosterone status, rather than engaging in self-defeating habits that will speed the decline in T levels. Alcohol abuse, recreational drug use, pharmaceutical drugs, stress, and poor sleep habits can all lower testosterone levels.

So too can low-fat diets.

Research shows that reducing fat intake from around forty percent to 20-25 percent of calories decreases testosterone output. Low fat diets also increase levels of sex hormone-binding globulin (SHBG), a protein which binds to testosterone, thus reducing the amount of bioavailable, or ‘free’, testosterone in the body. It is free testosterone that is responsible for this hormone’s favorable effects on growth, repair, sexual capacity and immune function(79-81).
Again, not just any old fat will suffice when it comes to optimizing testosterone levels. A study with weight-training men showed higher saturated fat and monounsaturated fat consumption to be positively associated with testosterone levels. In contrast, higher dietary levels of so-called “heart-healthy” polyunsaturated fats relative to saturated fats were associated with lower testosterone levels (82).

It’s highly ironic that athletes and bodybuilders will take all manner of expensive, esoteric and often dubious testosterone-boosting concoctions–not to mention anabolic steroids–yet will follow hormone-damping low-fat diets with religious fervor. It’s a little like putting on a weighted vest before a big race and expecting to run at full speed.

Hormones like testosterone play a fundamentally important role in stimulating and regulating growth and metabolism. Don’t go throwing a low-fat monkey wrench into your metabolic engine!

Low-Fat Diets and Immune Function

Diet ‘experts’ assure us that a low-fat diet is the key to good health. The published research does not support such claims.

Despite the virulent ranting of anti-fat activists, trials comparing sedentary adult volunteers fed low-fat diets with those receiving higher fat diets has shown no improvement in immune status in the former group(83,84).

In children, whole milk consumption is associated with fewer gastrointestinal infections than consumption of low fat milk (85). Rats consuming diets high in milk fat show a significantly greater resistance to Listeria infection and higher survival rates than those whose diets were low in milk fat(86). Similar results have been observed in mice fed diets high in saturate-rich coconut oil(87)

In athletes, who are constantly pushing their immune systems to the edge with strenuous training, adherence to the commonly-recommended low-fat high-carbohydrate diet (15-19% of total calories) increases pro-inflammatory immune factors, decreases anti-inflammatory factors, and depresses antioxidant status when compared to higher fat diets (30-50% of total calories)(88,89). Such changes may leave athletes on low-fat diets with a lowered resistance to infection and a higher risk of chronic illness. This may be due to difficulty in obtaining sufficient calories from low-fat diets to meet the energy demands of exercise; increasing dietary fat intake and total caloric intake to match energy expenditure appears to reverse the negative effects on immune function reported on calorie-deficient, low-fat diets. Diets comprising 32% to 55% fat also improve endurance capacity compared to diets with 15% fat(90).

It was Scandinavian researchers who, in the 1960s, performed research showing that using extremely high-carbohydrate, low-fat diets for short periods could enhance athletic performance. This was achieved by using these diets as part of a “depletion-repletion” carbohydrate-loading strategy, which helped temporarily elevate muscle glycogen stores to higher than usual levels. One of the pioneers in this area, Dr. Jan Karlsson, points out that such diets were never intended to be applied for more than 3-4 days. Karlsson and his colleagues openly lament that these diets are now employed for extended periods of time, and refer to the prolonged use of very high-carbohydrate/low-fat diets by athletes as “voluntary malnourishment”. They note that in Scandinavia, researchers use the term “Carbohydrate Trap” when referring to the widespread belief that these diets are required for optimal performance. These researchers consider a 50-55% carbohydrate, 35% fat diet to be eminently more sensible and nutritious than the >60% carb, <25% fat diets commonly used by athletes(91).

For athletes and non-athletes alike, the low-fat diet is a sick (pun intended) joke.

The Low-Fat Diet Does Not Protect Against Heart Disease, and May Actually Worsen It

The WHI trial confirmed what well-read cholesterol skeptics have known for a long time: The low-fat diet is a big fat fraud when it comes to preventing heart disease. Among the 48,835 women participating in the trial, no significant differences in CHD or stroke incidence, CHD or stroke mortality, or total mortality were observed(92). Nor were there any reductions in the incidence or mortality rates of breast cancer, colorectal cancer, or total cancer(93,94).
There was however, one very ominous finding to emerge from the WHI trial. Among the 3.4 percent of trial participants with pre-existing cardiovascular disease, those randomized to the low-fat diet experienced a 26% increase in the relative risk of non-fatal and fatal CHD!

Low-fat advocates have remained deafeningly silent on this inconvenient finding, and would no doubt like to believe this was just a ‘freak’ occurrence. However, this is hardly the first time that low-fat eating has been shown to worsen the prognosis of women with existing cardiovascular disease.

In 2004, the world’s most prominent nutrition journal, The American Journal of Clinical Nutrition, published the results of a very, very interesting study. Harvard researchers had taken 235 postmenopausal women with established coronary heart disease, and divided them into four categories according to their level of saturated fat intake. They then performed coronary angiographies at baseline and after a mean follow-up of 3.1 years, analyzing over 2,200 coronary artery segments in the process.

After adjusting for multiple confounders, a higher saturated fat intake was associated with less narrowing of the arteries and less progression of coronary atherosclerosis. Compared with a 0.22 mm narrowing in the lowest quartile of intake, there was a 0.10-mm narrowing in the second quartile, a 0.07 mm narrowing in the third quartile, and no narrowing in the fourth and highest quartile of saturated fat intake!

Following a low-fat diet means adopting a high-carbohydrate diet by default. After all, it is exceedingly difficult and highly unpalatable to achieve the bulk of one’s caloric needs by eating lean protein foods. It is of no small concern then, that carbohydrate intake was positively associated with atherosclerotic progression, particularly when the glycemic index was high. The intake of so-called ‘heart-healthy’ polyunsaturated fats was also positively associated with progression of atherosclerosis, but monounsaturated and total fat intakes were not associated with progression (it must be noted that the major sources of polyunsaturates in Western countries are refined vegetable oils which are rich in the omega-6 fat linoleic acid. The polyunsaturated omega-3 fats, which are underconsumed by most Westerners, have actually been shown to lower CVD).

After examining the baseline data for the study subjects, it is apparent that the results can not be explained away by otherwise healthier lifestyles among those eating the most saturated fat; the high saturated fat group, in fact, had the greatest number of current smokers! Women eating the most saturated fat were also less likely to take blood-thinning medications like aspirin(95).

If this study had found saturated fats to be associated with cardiovascular disease, its results would have been trumpeted in headlines around the world. Instead, they were largely ignored by the mainstream media and our ever-so responsible ‘health’ authorities. It appears only studies that support the cherished dogma of our health orthodoxy are considered suitable as press release fodder…

A major factor in the progression of cardiovascular disease–and most major diseases–is free radical damage. It is well-established that saturated fatty acids, because of their lack of vulnerable double bonds, are the least susceptible to free radical damage; polyunsaturates are the most vulnerable. We also know that increased carbohydrate consumption, especially of the refined variety, does an outstanding job of raising blood sugar and insulin levels, which accelerates glycation, free radical activity, blood clot formation, and arterial smooth muscle cell proliferation.

It should also be noted that increasing heart disease incidence throughout the twentieth century has been accompanied by increasing polyunsaturate consumption, while a marked increase in refined carbohydrate consumption during the last three decades has been accompanied by spiralling obesity and diabetes incidence. Animal fat consumption, in contrast, has remained stable over the last 100 years.

So what we have is two studies that show that women with pre-existing heart disease will experience WORSE outcomes if they shun saturated fat and opt for a low-fat/high-carbohydrate diet! Furthermore, the validity of these results is supported by basic biochemistry and epidemiological data. So will low-fat advocates stop recommending this pattern of eating to women with heart disease? Does their concern for human life override their need to defend their precious low-fat dogma at all costs?

I truly doubt it…

If low-fat advocates won’t be straight with you, then I will. Let’s be perfectly clear on this: If you are female, and suffer cardiovascular disease, the published, peer-reviewed scientific evidence indicates that adopting a low-fat diet could be DEADLY.

The WHI is not the only dietary intervention trial to demonstrate the worthlessness of the low-fat diet in preventing CVD. In 1965, the prominent journal Lancet published the results of a trial conducted by the UK Medical Research Committee. In this study, 264 men under 65 were assigned to either a low-fat diet or their usual diet. Dietary records show that those in the low-fat group averaged 45 g/day of fat throughout the trial, while those in the control group actually increased their average fat intake from 106 to 125g. The average serum cholesterol measurement of the low-fat group was 25 points lower than that of the control group at 4 years. Despite nonsensical claims that “every 1mg/dl drop in cholesterol equals a 2% drop in CHD risk”, there were no differences between the two groups in CHD incidence or mortality after 4 years.

In Search of the Elusive ‘Negative Fat Intake’!

The hysterical anti-fat vitriole that spews forth from some anti-fat faddists leads me to believe that if these clowns could eat a ‘negative-fat’ diet, they would! As for their argument that the above trials didn’t lower fat enough, one has to wonder how creating even greater deficiencies in valuable nutrients, and predisposing one to greater risk of depression and anger–all of which low-fat diets have indeed been clinically documented to do–will in any way help prevent heart disease! Maybe these folks have been eating low-fat so long that it’s started to drain their brains; healthy human brains, after all, are 60% fat by weight!

The authors of the MRC trial concluded that: “A low-fat diet has no place in the treatment of myocardial infarction.” Despite being written over forty years ago, these words have largely been ignored by a medical and health hierarchy which seems to earnestly believe that if only it keeps flogging the dead low-fat horse, it will one-day magically spring to life. In Australia, this is known as engaging in a ‘wank’, which means that people who push low-fat diets despite no proof whatsoever of their efficacy are wankers. This might be stating the obvious, but…you really shouldn’t listen to wankers!

But the Japanese Eat a Low-Fat Diet…Don’t They?

Supporters of low-fat nutrition cite the Japanese ad nauseum, claiming that their low-fat/high-carbohydrate diet is the reason for their low rate of heart disease. It is ironic that many of these same commentators exhort the benefits of whole-grains and tell us that the only ‘bad’ carbohydrates are those that come from refined sugars and grains. These folks need to get their story straight—a major source of carbohydrates in the Japanese diet is white rice–a refined grain! That means that if the high-carbohydrate Japanese diet is cardio-protective, then refined grains must be good for one’s heart! Well, which is it? You can’t have it both ways; either refined grains are heart-friendly, or they’re not!

The truth is, the longevity and low CHD incidence of the Japanese owes nothing to carbohydrate intake, refined or otherwise. During the 1960s and 1970s, industrialization underwent rapid growth in Japan. This period of marked economic change bought with it greater consumption of animal protein and fat. This increased animal food consumption in Japan has been accompanied by a marked decline in both the overall incidence of and the mortality from one of that nation’s biggest killers–stroke. This increase in animal protein and animal fat consumption has also occurred alongside Japan’s rise to the top of the longevity ladder.(96,97)

If you’re tempted to write this off as merely a consequence of improved living standards and medical technology, keep in mind that long-term follow-up studies with both native and migrant Japanese populations show that those who eat the most animal protein and animal fat enjoy greater longevity and a lower incidence of stroke than those who eat lesser amounts(98-101).

OK, So What About the Mediterranean Diet?

A diet low in saturated fat is purportedly a major factor in the low rates of CHD observed in Southern European countries. Just one wee problem: France, the Mediterranean country with the lowest CHD rates of all, is also the Mediterranean country with the highest saturated fat intake!

Oops!

Health ‘experts’ have tried to brush off this embarrassing observation as a ‘paradox’ (orthodoxy loves applying the ‘paradox’ label to uncomfortable contradictions) by claiming that red wine explains this difference. If that were true, then the Italians, who drink a similar amount of red wine, should have CHD rates even lower than France. But they don’t; their CHD rates are similar to those of other Southern European countries where far less red wine is consumed(102).

Conclusion

I could go on, and on, and on…but I’ll just close by saying that the low-fat diet has NEVER been demonstrated to do all the wonderful health-fortifying things claimed for it. The only trials showing favorable effects in people following low-fat diets are those that simultaneously employed other truly useful interventions, like exercise, stress management, increased fruit and vegetable intake and decreased processed food intake, and weight loss. However, there is absolutely no law whatsoever stating that low-fat eating is required for the implementation of any of these strategies. In fact, given the available evidence, one can only conclude that the inclusion of higher fat intakes in these trials may even have improved the results!

The bottom line: Not only is low-fat eating a boring way to go through life, it is a useless and often counterproductive hoax.

References and Assorted Disclaimers:
DISGRUNTLED WORSHIPPERS OF THE LOW-FAT RELIGION SHOULD READ THE FOLLOWING:I have not stated anything in this article that cannot be verified by published, peer-reviewed research. Nonetheless, my inbox will no doubt be flooded with angry emails from those who have been brainwashed by the low-fat paradigm, and who violently object to the thought that something that they have believed in so strongly for so long might actually be false. In other words, malevolent dimwits who want to shoot the messenger! For those of you who fall into this category, my suggestions are as follows: 1) GROW UP!; 2) Start placing a premium on discovering the facts, as opposed to doggedly defending what you have already decided you want to believe; 3) Instead of attacking me, start questioning the motives of those who profit greatly from the fallacious anti-fat, anti-cholesterol paradigm. This includes the food and drug conglomerates that make BILLIONS from the sale of low-fat foods and cholesterol-lowering drugs, the health and dietetic ‘associations/organizations/institutes/foundations/etc’ who receive millions in ‘donations’ from these very same companies, and the executives of these so-called ‘non-profit’ organizations who enjoy six-figure incomes and extensive perquisites.
To attack the owner of a non-commercial web site, who has nothing to gain financially by either supporting or opposing the low-fat paradigm, while defending those WHO DO, is so bloody stupid that it defies comprehension. Unfortunately, there are a lot of bloody stupid people in the world! If you are one of them, and decide to write me, please note that unless your email contains valid references to the scientific literature, it will be deleted immediately. After having established yourself as an ignorant goofball, your email address will also be added to my spam filter and any further emails will be delivered straight to my trash. Sorry, but I really am extremely busy and have no time or patience for ignorant, time-wasting twits.

NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first)! However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part. A hyperlink to www.TheOmnivore.com would also be greatly appreciated! Those wishing to reprint this or any other article on TheOmnivore.com for commercial purposes should email: ac.theomnivore@gmail.com

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What to Do About Inconvenient Facts?

“The great tragedy of Science — the slaying of a beautiful hypothesis by an ugly fact.”
— Thomas Huxley

So begins an article today in TSC Daily, Eating Some Crow on Fat, by John Luik.

The attitude of we-know-best-no-matter-what-the-studies-say discredits both the scientific process and the requirement that health advice be evidence-based. It risks turning off a population already weary and wary of the lifestyle solutions offered up by the medical community. And it ignores a fundamental responsibility that attaches to providing risk advice: If the science changes, amend your advice. To do otherwise changes the enterprise from advice-giving to propaganda-making. However beautiful the hypothesis, the “ugly” facts are always preferable.

It’s one of those articles you have to read – no need for analysis from me!

From the Fat Files

It’s amusing to read all the excuses advanced to dismiss the null findings from the WHI Dietary Modification Trial – my favorite is the one that claims that reducing fat is passe, that we’d moved on from that thinking about the time the study was just getting underway.

We find this excuse in a number of articles, but a quote in the International Herald Tribune in their article, Chances a low-fat diet will help? Slim and none, really is the best – “The diets studied “had an antique patina,” said Dr. Peter Libby, a cardiologist and professor at Harvard Medical School. These days, Libby said, most people have moved on from the idea of controlling total fat to the idea that people should eat different kinds of fat.”

Oh really? Then why are the studies still being published in the medical journals so focused on total fat?

Yesterday I wrote about a study published in November 2005, last week, a study published this month, and today, let’s take a look at one published in April 2004 – Effect of low and high fat diets on nutrient intakes and selected cardiovascular risk factors in sedentary men and women.

This one placed study subjects on two different diets – one that was just 19% fat and another than was an eye-popping 50% fat. Guess who did better? If you said those on the low-fat diet, you’re wrong. Those on the 50% fat diet increased their HDL-C to an amazing 63! The researchers noted that those on the low-fat diet may not be able to consume ENOUGH calories on such a diet, that the low-fat diet was deficient in essential fatty acids, missed essential micronutrients (especially zinc and Vitamin E) and also lowered ApoA1.

Guess the media missed that one too, huh?

Amazing when you think about it – the media only seems to find and provide information about studies that support the low-fat paradigm – and even when they do include one that clearly shows no benefit, they advance the message that something was wrong with the study – be it not enough time or those in the study just didn’t lower their fat enough!

How about another example that illustrates how diet can affect risk markers? Back in May 2003, the Tohoku Journal of Experimental Medicine published the findings of a study on diabetic patients – Effects of diet treatment on some biochemical and physiological parameters in patients with type 2 diabetes mellitus. The conclusions offer no real insight to what happened to those with diabetes: This study showed that diet treatment could not normalize the high systolic blood pressure in type 2 DM. Thus, an effective way of controlling blood pressure should be taken to improve healing in DM.

Want to know what really happened? Well, when they had their diet changed to 50-55% carbohydrate, 30% fat and 15-20% protein….heck I’m not afraid to tell you…

• Total Cholesterol – decreased from 231 to 227
• LDL – INCREASED from 139.4 to 150.9
• HDL – DECREASED from 44.4 to 40.2
• Triglycerides decreased from 290 to 192.4
• TC/HDL Ratio – INCREASED from 5.2 to 5.64 (an increase is BAD)
• Blood pressure – INCREASED from 114/87 to 139/85

Yet the best the researchers could conclude in their abstract was that the diet couldn’t normalize systolic blood pressure? Good grief – the diet intervention made these folks worse! Here though, the researchers did at least have the guts to state “Increasing fat intake to 50% of calories improved nutritional status, and did not negatively affect certain cardiovascular risk factors,” in the full-text portion of their paper.

Not a peep from the media though.

Not a word of caution to diabetics from the American Diabetes Association either.

Not even the review, published in the American Journal of Cardiology – High-density lipoprotein as a therapeutic target: clinical evidence and treatment strategies – received the attention it should have.

In it, the authors state, quite clearly, “The clinical importance of low serum levels of high-density lipoprotein (HDL) cholesterol is often under-recognized and underappreciated as a risk factor for premature atherosclerosis as well as for cardiovascular morbidity and mortality. Low serum levels of HDL are frequently encountered, especially in patients who are obese or have the metabolic syndrome. In prospective epidemiologic studies, every 1-mg/dL increase in HDL is associated with a 2% to 3% decrease in coronary artery disease risk, independent of low-density lipoprotein (LDL) cholesterol and triglyceride (TG) levels.”

Yet we continue to see the media and experts hone in our lowering of total cholesterol and LDL as beneficial even when the cited studies show a decrease in HDL and worse TC/HDL ratios! Folks, that’s NOT a benefit for long-term health.

If you haven’t started to notice, there are a number of studies out there that show we’re still looking in all the wrong places (trying to lower total fat intake) and that the contention that we’re long past that is way off base. We’re entrenched in it and still fail to appreciate how dietary fats – yes even the much maligned saturated fats – increase HDL while reducing the TC/HDL ratio, which is considered a good number to use to predict cardiovascular disease!

What Does Saturated Fat Do to Your Cholesterol?

The American Heart Association continues to advance the belief that saturated fat is bad for our hearts, and specifically recommends that we do our best to achieve a “desirable choleserol level” by a variety of dietary changes, including:

• Limit foods with a high content of saturated fat and cholesterol. Substitute with grains and unsaturated fat from vegetables, fish, legumes and nuts.
• Limit cholesterol to 300 milligrams (mg) a day for the general population, and 200 mg a day for those with heart disease or its risk factors.
• Include fat-free and low-fat dairy products, fish, legumes, poultry and lean meats.

A study was published last year in the American Journal of Clinical Nutrition (November 2005) that followed a group of 86-men, aged 22-64 eating three different diets. Meals were prepared for them to maintain compliance with the dietary changes and the fat content of each diet was manipulated by using different dairy products – full-fat, reduced fat and non-fat.

The results are quite telling about how saturated fats and our intake of dietary cholesterol affect our cholesterol.

Before we look at the findings, let’s see what the diets looked like:

The “Average American Diet” (ADD)

• 36.8% fat (14% SFA, 14.5% MUFA, 8.3% PUFA)
• 49.6% carbohydrate
• 13.6% protein
• 104mg cholesterol/1000 calories

The “Step I Diet”

• 28.1% fat (8.8% SFA, 11.5% MUFA, 7.9% PUFA)
• 58% carbohydrate
• 13.9% protein
• 76mg cholesterol/1000 calories

The “Step II Diet”

• 23.7% fat (6.2% SFA, 9.7% MUFA, 7.8% PUFA)
• 61.9% carbohydrate
• 14.4% protein
• 63mg cholesterol/1000 calories

All participants were fed an isocaloric diet to maintain their weight and the calorie levels ranged from 2200-3400 since each participant ate what they needed to maintain their weight. If their weight fluctuated more than 1kg, their diet was adjusted until their weight returned to their intial weight. This is an important factor in this study – the men were neither allowed to gain or lose weight during the intervention periods. What this allows is a clean look at how dietary fat is impacting various measures of health without the confounding variable of weight change.

At baseline, the men had an average

• Total Cholesterol = 186.34
• LDL Cholesterol = 126.41
• HDL Cholesterol = 40.20
• Triglycerides = 96.57
• TC/HDL Ratio = 4.63

And, let’s be clear – these guys were pretty average…the average BMI was 25.6 (range was 22-33.2)

Wonder what each diet did to their cholesterol levels? Well, you might be surprised….

The Step II Diet (the one you might think was the healthiest) did the worst, even though it effectively lowered total cholesterol the most, from 186.34 to 169.71. LDL was reduced from 126.41 to 110.95, but HDL was also reduced from 40.20 to 36.72 and triglycerides rose from 96.57 to 108.09.

The Step I Diet fared slightly better, but still wasn’t an improvement when we take a close look. Total cholesterol declined from 186.34 to 177.44 with LDL decreasing from 126.41 to 117.13 – but again, the diet also took it’s toll on HDL, causing it to decrease from 40.20 to 38.27. Triglycerides also rose from 96.57 to 106.32.

The real surprise was that the ADD diet actually made some improvements in cholesterol. Total cholesterol remained 186.34, but LDL declined slightly to 125.64 and HDL rose from 40.20 to 41.36, while triglycerides declined from 96.57 to 93.91.

The researchers did a number of analysis – in the hope to find some redeeming value for the low-fat diets – to no avail. No matter how hard they looked, no matter what parameter they analyzed (from BMI to glucose, from insulin to waist circumferance, from body fat percentage to HOMA score) the lower fat diets performed poorly.

You wouldn’t know that from the abstract though – in it the researchers merely conclude “Persons who are insulin resistant respond less favorably to Step II diets than do those who are insulin sensitive.”

Noteworthy in the full-text of the paper is this observation from the researchers – “Being overweight and the associated insulin resistance that can lead to the metabolic syndrome is a growing health problem. Only 7% of our study population met the criteria for having metabolic syndrome as defined by National Cholesterol Education Program. Nonetheless, the participants who were overweight or who had higher insulin concentrations had altered metabolic responses to lower fat diets. Thus, the effects of elevated insulin concentrations on the LDL-cholesterol and triacylglycerol responses preceded the development of overt metabolic syndrome.”

It’s estimated that 25% of Americans already are affected by the features of Metabolic Syndrome – this particular study only had 7% within its subjects, and yet – even before they met the criteria for Metabolic Syndrome – if they were overweight and had higher insulin concentrations, the Step I and Step II Diets were bad news for their cholesterol!

If you recall, this was published in November 2005 – just three months ago. This month we had the Women’s Health Initiative Dietary Modification Trial show that low-fat diets did not improve cholesterol or reduce the risk of breast cancer, colon cancer or cardiovascular disease. There are many other studies out there too that have resulted in similar findings. Yet, the AHA and others continue to march to the beat of dogma instead of evidence-based standards.

In an editorial regarding this study, the author, Jose Ordovas, notes this when he wrote “These results were, on average, similar to those from many previous studies that used similar experimental designs and diets.”

Ordovas continues later with “The other relevant outcome of the study relates to the results obtained for the ratio of total to HDL cholesterol, also known as the atherogenic ratio. Higher values have been associated with an increased CVD risk. Therefore, the elevations observed after the Step I and II diets cast some concerns about the efficacy of these low-fat diets to reduce CVD risk.”

He then quickly retreats however, and instead looks to call the study design into question “However, experimental design may have been the driving force for the increased ratio of total to HDL cholesterol and triacylglycerol concentrations observed after the low-fat diets,” even though he’d previously praised the design earlier “Lefevre et al’s study design fulfills many of the expectations of a well-conducted dietary intervention study, namely, a randomized, double-blind, 3-period crossover controlled feeding design. In addition, these investigators take multiple measurements per dietary phase, which reduces the confounding of intraindividual variability. Moreover, they chemically measured the menus provided, thereby connecting the calculated with the actual composition of the diets.”

He ends by saying that “the first baby steps can be seen already in the most current version of the US Department of Agriculture pyramid (www.mypyramid.gov). Perhaps at some time in the future, the current controversies will be put to rest. We will be able to identify those persons for whom diet plays no major role in their risk of CVD and this should appease those who defend the diet-heart null hypothesis. The same tools will identify those persons who may benefit more from one of the many potentially beneficial diets currently proposed.”

This leads a reader to believe that someone in the study, on the Step I or Step II Diets, actually saw an improvement in their cholesterol! There is no data to suggest such a leap of faith.

Basically, he tows the line and maintains the message that the Dietary Guidelines for Americans (DGA), which is close to the Step I Diet, is just fine and dandy.

This study, taken with the number of other studies that have reached similar findings should be reason enough to demand we cease-and-desist with these guidelines. With 25% of the adult population already presenting features of Metabolic Syndrome, such dietary recommendations will continue to exacerbate the problem, not make things better.

Folks, just look at the data for yourself – reducing your saturated fats and using “good” monounsaturated and polyunsaturated instead, even lowering your total fat – does nothing to improve your cholesterol! Using low-fat and fat-free dairy in place of whole milk dairy – that too does nothing to improve your cholesterol! Lowering your intake of dietary cholesterol – yup, that too does nothing to improve your cholesterol. But you wouldn’t know that if you listen to the “experts” and don’t read the data for yourself, would you?

Low-Carb – High-Carb – Protein…What Does the Data Tell Us?

One of the largest meta-regressions to review the effects of low-to-moderate carbohydrate diets was published this month in the American Journal of Clinical Nutrition, Effects of variation in protein and carbohydrate intake on body mass and composition during energy restriction: a meta-regression. This particular review has received no mention in the press – most likely because the null findings from the WHI Dietary Modification Trial continues to dominate the headlines.

It’s an important review however, bringing together a comprehensive and impressive set of data – 87 studies made the cut and were included in the analysis. Oh, and I think it’s important to note, the researchers in this study – from the Department of Food Science and Human Nutrition and of Statistics, University of Florida – none have previously published studies investigating low-carb diets or low-fat diets. Noteable too is the conflict-of-interest disclosure – the paper was not the product of any outside funding – in fact, the paper states the lead researcher, James W Krieger, funded the effort.

So, then, let’s get to the good stuff – what the researchers wanted to know and what they found when they started looking at all this data! They reviewed a number of factors:

• Body mass change
• Fat-free mass change
• Percentage changes in body fat
• Fat mass changes

After this comprehensive review and analysis, their conclusion was “Low-carbohydrate, high-protein diets favorably affect body mass and composition independent of energy intake, which in part supports the proposed metabolic advantage of these diets.”

Body mass change

Diets with carbohydrate intake in the lowest quartile were associated with a 1.6–1.7kg greater body-mass loss than were diets with carbohydrate intake in the highest 3 quartiles. When carbohydrate intake was categorized as low or high, the significant effect in the low-carbohydrate intake group remained.

Fat-free mass (FFM) change

The amount of FFM retained tended to increase with each successive quartile of protein intake, with a significant difference existing between the upper 2 quartiles (greater than 1.05g/kg) and the first quartile (0.7g/kg). Specifically, the third quartile ( greater than 1.05 and 1.2g/kg) was associated with 0.78kg additional FFM retention and the fourth quartile (greater than 1.2g/kg) was associated with 0.96kg additional FFM retention.

Compared with carbohydrate intake in the lowest quartile, the carbohydrate intake in the highest quartile was associated with 0.98kg greater FFM retention. Carbohydrate intake in the second and third quartiles tended to be associated with 0.62–0.65kg more FFM retention.

In their discussion, the researchers state “Protein intake was a significant predictor of FFM retention. A daily protein intake of greater than 1.05g/kg was associated with a greater FFM retention than was a protein intake closer to the RDA. The magnitude of this effect increased when studies of greater than 3-mo duration were analyzed. Thus, the protein RDA may not be optimal for FFM retention during energy restriction, particularly during prolonged periods of dieting. Energy restriction can decrease nitrogen balance and thus decrease the amount of protein and FFM retained by the body. An increase in protein intake would increase nitrogen balance and thus increase the amount of FFM retained.”

Percentage changes in body fat (BF)

Diets with a carbohydrate intake in the lowest quartile were associated with a 1.32–1.48% greater decrease in percentage BF than were diets with carbohydrate intake in the highest 3 quartiles. When carbohydrate intake was categorized as low or high, the significantly greater decrease in percentage BF in the low-carbohydrate intake group remained.

Fat mass (FM) changes

Diets with carbohydrate intake in the lowest quartile were associated with a 1.79–2.32kg greater loss of FM than were diets with carbohydrate intake in the highest 3 quartiles. When carbohydrate intake was categorized as low or high, low-carbohydrate diets were associated with a greater loss of FM than were high-carbohydrate diets.

One claim often made by those who insist that low-carb diets are not effective is the contention that weight loss is just water loss. Here, the researchers are clear – “Compared with higher carbohydrate intakes, low-carbohydrate diets increased the loss of body mass, BF, and percentage BF, even after control for energy intake as a covariate in the regression analyses. The mean total carbohydrate intake in the low-carbohydrate studies ranged from 79g–97g, depending on the analysis. Typically, a carbohydrate intake of less than 100g will cause ketosis. These results support the apparent metabolic advantage of low-carbohydrate, ketogenic diets. The additional body mass change is not likely due to water loss, because the duration of the diet periods (6–24 wk) was too protracted and estimations of total body water tend to be similar between low-carbohydrate and low-fat diets after 2-wk. The similar results of the analyses on body mass and BF also supports the concept that the effect on body mass of low-carbohydrate diets is an effect on FM rather than on body water.”

At the end of their discussion, the researchers – a second time – make a bold statement – In conclusion, low-carbohydrate diets may increase the loss of body mass, FFM, FM, and percentage BF during weight reduction compared with traditional diets. The RDA for protein may be insufficient for optimal FFM retention during weight loss; high protein intakes (greater than 1.05g/kg) may improve FFM retention.

The researchers did a good job of selecting studies and weeding out those that did not meet their inclusion criteria. If you recall, last week I wrote about how poor data results in useless analysis in my article Comparing Low-Carb to Low-Fat: Analyzing a review. A quality review requires quality data – quality data comes from participants actually sticking with a particular dietary approach.

More importantly, this particular review highlights the importance of protein intake. The researchers took the additional step to analyze not percentage of calories, but actual gram intake in each study. This approach allowed us to gain a better understanding of how critical protein is in our diet. Those consuming protein at the RDA did much worse than those consuming a higher protein intake.

The review puts the spotlight on just how important protein consumption is when you’re following a weight loss diet – higher in carbohydrate or lower in carbohydrate – protein is a critical, essential nutrient and if you reduce your intake of protein, you’ll lose more lean body mass. This fact is all the more obvious in this review and calls into question, once again, the standard recommendation to consume protein as a percentage of calories (10-15%) while trying to lose weight. As I’ve pointed out a number of times – following that advice reduces protein intake dramatically – something this paper clearly shows is detrimental to lean body mass in weight loss regardless of carbohydrate intake.

Let’s not forget, protein isn’t just an essential nutrient – it also offers a higher degree of satiety when one is trying to lose weight too!Take away message from this review – low-carb diets work, they do have a metabolic advantage and it’s critical to make sure you’re eating enough protein each day while keeping your carbohydrate intake low!

In the Thin – Why Calories May Not Matter

In the article, Study: Watching Calories Takes Commitment, there’s no mention of the various letters challenging the study findings as they relate to humans. In fact, a read of the article will leave you with the impression that the author’s concluded that calorie restriction will extend your life span. In their published studies, they didn’t reach that conclusion – in fact, they reported their findings as relevant to primate species and were careful not to extend their findings to homo sapien.

More troubling though is the Washington Post article statement that “Losing that extra weight is one thing. Keeping it off requires a lifetime of counting calories,” followed two sentences later with “Genetic differences allow some primates to remain thin and others to grow fat when fed an identical diet over the years, the study found.”

So, which is – did the thin monkeys have to restrict calories or not to remain thin? Apparently not – some grew heavier with an IDENTICAL diet as their thinner counterparts. Somehow that’s totally lost in the article and we’re told instead that only a lifetime of counting calories is going to keep us slim. On identical calories some grew fatter than others. The researchers chalked that up to genetic differences. The author of the article decided that calorie restriction solves that problem.

What’s missing?

Discussion of the metabolic changes that were going on in those monkeys that grew heavier on the same diet – loss of insulin sensitivity, rising blood sugars, rising insulin levels, diabetes. In fact, insulin sensitivity, or lack thereof, was the leading predictor of death in the monkeys. As the study abstract states, “Hyperinsulinemia led to a 3.7-fold increased risk of death (p = less than 0.05);”

That’s not specifically genetic – that’s a specific metabolic process going awry.

Might genetics play a role in such declines in metabolic function? Absolutely.

Might it be something else, like the burden of long-term diet that may be inappropriate? Absolutely.

Might it be something else, like a combination of factors aligning to create a metabolic nightmare like the Perfect Storm? Absolutely.

We just don’t know all the answers at this point in time.

We certainly have clues – and when it comes to humans, we know how deadly high blood sugars, hyperinsulinemia and metabolic syndrome are. Reversing these conditions can be as simple as changing your diet to limit carbohydrate consumption to limit the insulin response to high blood sugars and thus increase insulin sensitivity. Often, the result of carbohydrate restriction is a spontaneous reduction in calorie intake – that is, it happens without effort to restrict calories. That often leads to weight loss, increased insulin sensitivity and overall improvements to risk factors.

Yet, this fairly simple approach is not the standard of care – instead we insist one must eat a low-fat, carbohydrate rich diet to avoid that nasty fat, use an assortment of pharmaceutical interventions to “treat” the symptoms and manage insulin levels, and watch helplessly as the inevitable happens – decline and degradation of the body.

Calorie restriction may alleviate some of the symptoms, but it’s not reversing the condition, it’s not addressing the root problem – high blood sugars. To fully tackle that issue in the metabolism, only one thing effectively works without drugs – restricting carbohydrate!

Should We Dismiss Evidence for the Hypothetical?

Sooner or later it was bound to happen – someone, somewhere would address the issue of economic factors if we abandon the decades old high carbohydrate, low fat recommendations. This month, in the American Journal of Clinical Nutrition, several Letters to the Editor appeared regarding the study by Weigle et al in July 2005, A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations.

For those who didn’t read about the study last July – the researchers found that increasing protein in the diet to 30% of calories led to a spontaneous reduction in calorie intake, even when carbohydrate was constant, even with a reduction of fat intake, and resulted in significant weight loss when compared with a traditional macronutrient mix that provides 15% of calories from protein.

In their letter, Franco Contaldo and Fabrizio Pasanisi, write:

Weigle et al raise the intriguing question of whether high-protein diets are useful in preventing and treating excess body fat – a clinical issue that affects more than one billion people. They showed that a high protein intake reduces body weight by increasing satiety. Their study, together with the editorial by Astrup, raises the question of whether high-protein diets should be promoted in large numbers of people, particularly given the high protein intake typical of Western diets. Suffice it to note that the current estimated protein intake in the United States is already more than double the recommended amount. As a matter of fact, the human species is omnivorous and has developed very efficient adaptive physiologic mechanisms for fuel utilization, notwithstanding the feast or famine pendulum and that meat constituted the staple diet of our pre-Neolithic ancestors.

However, a meat-based diet – which has a high protein content – is largely less environmentally sustainable than is a vegetarian-based diet nowadays. A meat-based diet had little effect when the world’s population numbered only a few million, unlike today when more than 6 billion individuals are competing for resources. Furthermore, a high-protein diet may have untoward effects, for example, on calcium and bone metabolism.

In conclusion, the findings reported by Weigle et al confirm some basic physiologic concepts of human nutrition; a high-protein diet can have untoward effects, may be difficult to adhere to, and, most importantly, is not environmentally sustainable. Thus, caution should be exercised in applying the findings of Weigle et al in the clinical setting.

Noteworthy here is that Cantaldo and Pasanisi actually admit in their letter than meat was the staple diet for our ancestors. They then move along to the logical reason to dismiss this – today we simply cannot sustain such a diet population-wide in the United States nor the world, and that such a diet would be an environmental nightmare and lead to competition for resources.

Since when do we ignore evidence and data that inconveniently impacts “policy”? Since when is our data, that supports a different macronutrient mix than we’re recommending, have to be weighed against economic impact rather than health outcome?

Just who would be affected if we were to strictly use just evidence – not opinion, not feel-good policy making and not impacts the evidence might have – just the facts, just the data that relates to what really matters – our health. Well for one, we’d all be a heck of a lot healthier if we started to follow the science and not the opinions and entrenched dogma.

Let’s put that aside for a moment though – Cantaldo and Pasanisi bring up something else that sounds so ominous…a higher protein diet won’t just be an environmental nightmare, it would also untoward effects…on calcium and bone metabolism. They even provide references to show they have scientific evidence to support their contention!

Their choice of references is very, very interesting:

Eaton SB, Konner M. Paleolithic nutrition. A consideration of its nature and current implications. N Engl J Med 1985; 312: 283–9.
AND
Kerstetter JE, O’Brien KO, Insogna KL. Low protein intake: the impact on calcium and bone homeostasis in humans. J Nutr 2003; 133(suppl): 855S–61S.

I doubt they thought anyone might actually read their references – both support a higher protein intake is not detrimental for health. Eaton et al provides insight that our ancestors diet included 30% of calories from protein; Kerstetter et al provides good data about the detrimental effect of low protein intake, specifically on bone and calcium!

In fact, Kerstetter et al states in their paper, “The long-term consequences of these low protein–induced changes in calcium metabolism are not known, but they could be detrimental to skeletal health. Several recent epidemiological studies demonstrate reduced bone density and increased rates of bone loss in individuals habitually consuming low protein diets.”

To be clear, “low-protein” in their study was 0.7g protein/kg, the “high-protein” arms of the study consumed 1.0-2.1g protein/kg without detriment.

In their summary, they stated “There is agreement that diets moderate in protein (in the approximate range of 1.0 to 1.5 g protein/kg) are associated with normal calcium metabolism and presumably do not alter skeletal homeostasis.”

Part of their reason for the letter to the editor was also Arne Astrup’s editorial that accompanied the publication of the Weigel study findings that acknowledged a diet with higher protein has much potential to reverse the obesity epidemic we’re in. In fact, he wrote, “The higher than usually recommended protein content of many popular diets, such as the Atkins Diet, The Zone, and The South Beach Diet, seems to point at possible solutions to the obesity epidemic. Many national dietary guidelines have, until recently, recommended that only 10–20% of the calorie content of the diet come from protein; however, 30–40% of the calorie content in the aforementioned diets comes from protein, at the expense of carbohydrates. Newer research indicates that the high-protein content of these diets may actually be the reason for their partial success in inducing weight loss, despite no restrictions in total calories.”

In his rebuttal to Cantaldo and Pasanisi, however, he retreats slightly while trying to maintain some ground in support of higher protein diets, “In no way do I wish to suggest that overweight and obesity are “protein-deficiency conditions,” but increasing the proportion of protein in the diet may be one way to attenuate the obesity problem in a sedentary population and, thereby, to help reduce many of the obesity-associated comorbidities. Current evidence from experimental and intervention studies suggests that an increase in the amount of energy provided by protein from the current 15–18% in most diets to 20–35% is associated with a spontaneous reduction in total energy intake and a weight loss of relevance for obese and diabetic subjects.”

He adds, “In my editorial I mainly addressed the potential health benefits of increasing the proportion of dietary energy provided by protein at the expense of a reduction in fat and carbohydrate sources that are less satiating. I can only agree that many other issues need to be taken into account, such as safety aspects, economy, and environmental issues, before such recommendations should be made.”

Quite frankly, dietary recommendations should not be based on anything but nutrition science, quality data and evidence. Yes, the environment in important. Yes our economy is important. And, yes, safety is also important. But, when scientists abandon the evidence and weigh in on what are policy issues, we no longer are guided by evidence, no longer committed to our mission of “evidence-based medicine” – instead, we’re trapped by opinon and making decisions based on things not supported by the hard data.

This is dangerous territory for the scientific and medical communities – they risk ignoring their data to mold findings to meet politically correct opinions, long standing assumptions and economic policy. Researchers are not, and should not be charged with responsibility to solve all issues related to their findings, especially ones that impact the economy or environment. Such considerations are best left to the policy makers who are accountable to the public for economic stability and environmental sustainability.

The public deserves to have full disclosure of all the available evidence and not have its scientists carefully releasing only what is within current sustainability models or will not rock the economic boat. That’s not science, that’s manipulating things to fit the established paradigm and maintain the status quo – which, if you haven’t noticed has made us fatter and sicker over the last three decades!

When our future health takes a backseat and our review of the evidence is held hostage to outside considerations that are not related to the data, we’re in trouble. We’ve been doing this tap-dance since the early 70’s and it’s really time to stop and get back to the business of establishing dietary recommendations based on science, not economic consequences that remain hypothetical.

The alarmists who sound the warnings that we cannot sustain a higher protein diet – cannot feed ourselves such a diet let alone the entire world – and insist that such a shift would be disasterous to the environment fail to address the current situation where we’re already depleting our soil and water resources, while at the same time contaminating our foods with pesticides and chemicals and already in an unsustainable situation!

If we’re to get anywhere near establishing evidence-based nutritional standards, we’re going to have to set aside concerns for the environment and economy and review the data on its own, without consideration for anything else but our long-term health and how our nutritional policy enhances or thwarts our health outcomes. If we do that, then we have a chance to really put together economic and environmental policies that will support and sustain us in the years to come. Trying to do it the other way around – that is molding the evidence to our current economic and environmental policies – is sheer madness without any hope of better health outcomes.

What Does Saturated Fat do to your Blood Pressure?

With all the hubub surrounding the null findings for risk reduction with a low-fat diet in the WHI Dietary Modification Trial, some other interesting research is being overlooked. This month, the American Journal of Clinical Nutrition published Effects of dietary saturated, monounsaturated, and n–3 fatty acids on blood pressure in healthy subjects.

Researchers recruited 162 healthy subjects who were randomly assigned to one of two diets – high in saturated fat (SFA) or high in monounsaturated fat (MUFA). Both diets were isoenergetic (meaning enough calories to maintain the participants weight) and contained similar macronutrient distribution – 37% total fat, 15% protein and 43% carbohydrate.

Both groups were then randomized into two more groups – one group in each diet would also take supplements of omega-3 fatty acids while the other simply took a placebo.In the high saturated fat dieters, saturated fat intake was targeted to be 17% of energy daily, MUFA another 14% and PUFA 6%. In the high MUFA dieters, saturated fat was targeted to be 8% of energy, MUFA 23% and PUFA 6%.

The stated objective of the researchers: to evaluate the effects of different types of dietary fat on BP in healthy subjects.

Their conclusions: Changing the proportions of dietary fat by decreasing SFAs and increasing MUFAs decreased diastolic BP. Interestingly, the beneficial effect on BP induced by fat quality was negated by the consumption of a high total fat intake. The addition of n–3 fatty acids to the diet had no significant effect on BP.

Nary a word about how the high SFA group did.

Do you want to know? I did, so I took the time to read through the full-text and data tables….imagine my surprise when tucked in there was a statistically significant change in those eating a high saturated fat diet with more than 37% of their calories from total fat!

While it was true that there was a statistically significant decrase in diastolic blood pressure (your lower number) with the high MUFA diet in those who didn’t reach 37% of total calories from fat each day (p = 0.016), there was NO statistically significant change in systolic pressure (p = 0.152).

Sorry, no dice – high MUFA in a diet with 37% or less fat didn’t do all that much…

In reading the abstract conclusion, you’d probably walk away thinking the SFA group did poorly, huh?

Well, get a load of this….

In those consuming MORE than 37% of their total calories from fat, with a high saturated fat intake their decrease in diastolic blood pressure was significant too (p = 0.014) – more significant than those eating less than 37% total calories on the high MUFA diet (p = 0.016).

Not only that, but those eating more than 37% of their total calories from fat on the high SFA diet almost reached statistical significance with the decrease in their systolic blood pressure (p = 0.0524).

I say “almost” because the “p value” technically remains greater than 0.05, which is what you go by with a CI of 95%.

I didn’t round the result – if I had, I could have deceived you and just said it was just 0.05, technically correct – but that wouldn’t be all that honest, would it?

Do you want to know what else, besides saturated fat, the dieters eating the high SFA diet consumed? Cholesterol. Yup – more cholesterol – 322mg per day (+/-91mg).

Just one more example of how what’s stated in the abstract isn’t the whole story behind a study and it’s data…..

Life Expectancy – Beyond the Statistics

Today I received a number of emails asking questions about my article yesterday, The Fat Facts – Oh How We Eat!, and pointing out that back then life expectancy in the early 20th century was just about 50 years.

Ahhh, the statistics of life expectancy!

Life expectancy is a tricky thing to get a good handle on – for example, we know that back in 1910 the average life expectancy at birth was just about 50-years. At the time, that was true – and the years expected to live was based on what the population could expect at the time. What the statistic doesn’t show us though is how many people actually lived beyond that age or why.

The 1910 census tells us that there were 91.6-million people in the United States and 11.6% were age 65 or older. Yes, in 1910 that many people, born in or before 1845 managed to survive to at least age 65….they survived infectious disease, accidents, poor hygiene and the other obstacles of the day. In that year, 4% of the population was age 85 or older….these folks were born in or before 1825! The life expectancy in 1850 was just 39-years! For those who managed to live to 85-years old in 1910, they had another 4-years on average in their life expectancy – put another way, odds were good they’d live to 89.

Those actually born in 1910 actually saw little change in their life expectancy compared with those born in 1850 if they survived to age 40. Those born in 1850 who survived to 40 had a life expectancy of 69 years, those born in 1910 who reached 40 had a life expectancy of 68 years. Little changed for either population who reached 60 years old. Those born in 1850 could expect to live to 74, those born in 1910 could expect to live to 74.

So, how are we doing now? Pretty good. Someone who was 40 years old in 2003 can expect to live to 79 – ten more years than those born in 1850 or 1910. A 60 year old in 2003 can expect to live until they’re 82 – twelve more years than older generations. Where things really haven’t changed dramatically is in life expectancy for those who reach 70 and 80. If one was 70 in 1910, odds were good they’d live to 78….if they were 80, odds were in their favor they’d live to 85 or older. In 2003, a 70 year old had a good chance to live to 83 (five years more than in 1910) and an 80 year old had a good chance they’d live to 88 or older (three more years), those who reached 85 are expected to live until 89 (the same as 1910).

Prior to 1950, increasing life expectancy was mainly due to more children surviving childhood, a greater understanding of proper hygiene and improvements in the workplace for young adults which resulted in fewer accidental deaths. Since 1950, life expectancy increases are due to better healthcare, especially care of adults who reach 40 years or older – basically medical screening and treatment is undeniably better now than it was 60 years ago – and there is a much broader access to healthcare across the population. The greatest advance in longevity is really in those who reach age 60…but this longer life expectancy trend levels off pretty much the same once one lives to 80 as it has in the past.

I’m not trying to confuse here – it’s just that when you hear that in 1910 people lived an average of 50 years and today we live an average of 80, it sounds like we’re living much much longer. What we’re doing better, in reality, is keeping our kids alive in childhood and giving them better odds of hitting 40. If they reach 40, they do have a distinct advantage over those born in previous generations due in part to greater access to healthcare….but by the time they’re 70 that starts to level off and by 80 there really isn’t all that much difference in life expectancy between someone who was 80 in 1910 compared with someone who was 80 in 2003, someone with radically improved medical technology and access to care – remember, back in 1910, few seniors had health insurance!

In our determination to unlock the secrets of longer life, let’s not forget how important quality of life must be – if we’re going to live longer, shouldn’t we try to live in good health too? We’ve done a fantastic job improving the lives of our children (and the survival of women in childbirth) along with tackling many things considered “background” causes of mortality (violence, accident and some infectious disease)…we still need improvement in what’s called “senescent” causes of mortality – diseases and conditions that impact our health that rise sharply as we age, like cardiovascular disease and cancer. Between 1850 and 2000 we’d increased life expectancy at birth from 40.9-years to 80.8-years….between 1850 and 2000, the change in “senescent” life expectancy only increased from 72.6-years to 81.9-years. Since 1979 we’ve improved life expectancy for those who reach 60 years of age by just over one year, from 78.3 in 1979 to ….79.8 in 2003. Sadly, at the same time, years in “ill-health” has increased too, from six years in 1979, to more than nine, with women in 2003 averaging 10.7 years in ill-health and men averaging 8 years in ill-health. We’re living longer, but we’re not living as well when it comes to our quality of health declines in our later years.

And let’s not forget something that is more telling – humans actually have the potential to have a maximum lifespan of about 125 years. Robert Mitchell, professor of biology at Penn State has said, “We have to distinguish between maximum lifespan, which is as long as any human has ever lived, and life expectancy, which is how long you could live predictably, based on insurance statistics, for example. As far as maximum lifespan goes, we suspect it’s around 125 years. There is no evidence that humans can live any longer than that.”

History provides us with insight into a number of people who’ve lived past 100-years. The longest lived human (verifiable) was a French woman – Jeanne Calmet – died in 1997 at the age of 122, and she even smoked until she was 119 and finally gave up the habit when she grew tired of asking others to light her cigarrettes for her due to her declining eyesight.

If we have the potential to live to be 125 – in decent health – why are we not seeing rapid improvements in our average life span to reach our potential? In years gone by it was a matter of living through childhood, infectious diseases and avoiding accidents that mattered – if you could make it to 40 you’d probably make it to 70…..today if you make it to 40, even with all of our advancements, you’ll only likely make it to 80 – an increase of just ten years over what’s almost a century of progress.

Most promising today is research that is investigating the aging process of humans and other animals – specifically how well our body system repairs damage. The better we can repair cellular damage, from things like oxidative stress, the longer we live.

Research published in 1998, in the Journal of Comparitive Physiology – The rate of free radical production as a determinant of the rate of aging: evidence from the comparative approach – found that “Available research indicates there are at least two main characteristics of longevous species: a high rate of DNA repair together with a low rate of free radical production near DNA.”

What causes the damage and stimulates the repair cycle?

Well, for that, you’ll have to do some reading:

Damage-Based Theories of Aging

Enjoy!

The Fat Facts – Oh How We Eat!

The USDA is rich with information for anyone with some time to dig, click and follow the PDF’s, excel spreadsheets and other data put out for all to see. All I can say is this – it’s amazing how our diet has changed over the years – especially our use of added fats in our diet, either by our own use or the fats/oils used in food manufacturing.

Did you know, back in 1909 the average person in the United States consumed an eye-popping 83.68-pounds of animal fats a year? That’s more than a pound-and-a-half a week! Back then lard was the largest single source of fat/oils in the American diet, followed by butter. We consumed just 16.89-pounds of vegetable oils each year way back when.

That all changed in 1953, when soybean oil and products containing soybean oil displaced lard as the leader in the United States. We were on a roll replacing animal fats long before it was en vogue!

In 1960, the per capita consumption of animal fats fell to just 13.6-pounds per person, fell again by 1970 to just 8.9-pounds per person, and again in 1980 to 7.2-pounds per person. By 1990, we’d virtually eliminated animal fats from our diet, when per capita consumption hit an all time low of just 5.9-pounds per person!

During the same period our consumption of vegetable oils has skyrocketed – in 1960 we’d already increased our consumption to 31.6-pounds per capita, in 1970 another increase, this time to 43.8-pounds, and again in 1980 up to 49.9-pounds! Who-hoo we really hit the jackpot in 1990 when we hit 56.9-pounds per person annually!

In 1998 a report issued by the USDA, Have we Turned the Corner on Fat Consumption? stated that in 1997 consumption overall fell from 65.8-pounds annually to 65.6-pounds annually per person in the US. Also noted was that this decline in consumption was an unprecedented fourth consecutive year of decline.

By 1997, we really had altered our diet dramatically – dramatically less animal fat and even with vegetable oil replacing some of our animal fat, still an overall reduction of our intake – from more than 100-pounds of fats and oils in 1909 to just 65.6-pounds in 1997!

Just how different are we eating?

1909
Animal Fats = 83.68-pounds
Vegetable Oils = 16.89-pounds

1997
Animal Fats = 8-pounds
Vegetable Oils = 57.6-pounds

Even by 2000 we were still reducing animal fats and increasing vegetable oils:

2000
Animal Fats = 6.4-pounds
Vegetable Oils = 66.6-pounds

Why then are we not in the middle of virtual uptopia for health and well-being with the undeniable 93% reduction in our intake of animal fats since 1909?

We’ve been dutifully replacing those nasty, nasty saturated fats (so we’re told) with vegetable oils – an almost 4-fold increase in consumption since 1909. Heck, the Soybean Growers Association even boasts that soybean oil and soybean oil products now accounts for 80% of all vegetable oil consumed in the United States!

Why is no one asking why our obvious shunning of animal fats and increase in vegetable oils IS NOT working to provide a health benefit or reduce our risk of disease?

Could it be even remotely possible that we got it wrong in our thinking that saturated fats are deadly?

Could it be even remotely possible that we’re on the wrong track encouraging the population to eat even more vegetable oil and reduce even more their intake of animal fats?

Are you willing to bet your health that the “experts” are absolutely correct and that vegetable oils are better for you?

Toilet Water Cleaner than Ice in Restaurants

For the gross news of the day – a twelve year old schoolgirl, Jasmine Roberts, took part in a science fair at the New Tampa school and took the top prize for her project that compared the level of bacteria found in ice used in drinks served at a fast food restaurant with the level of bacteria in the toilets at the restaurant.

Her discovery: Seventy percent of the time, the ice had more bacteria than the toilet water.

In the article about her project, Girl’s Science Project May Make You Rethink That Drink Order, we learn that “For this project, Jasmine visited five fast food restaurants near the University of South Florida. She collected ice samples from self-service dispensers inside the restaurants, as well as ice from drinks served through drive-through windows. She also collected samples of toilet water from those restaurants.

She placed the samples into sterile containers and tested them at a lab at the H. Lee Moffitt Cancer Center, where she volunteers with a USF professor.

Jasmine found that in four of the five restaurants, the ice that came from the self-serve machines had more bacteria than the toilet water. Three of the five cups of ice from the drive-through windows had more bacteria than the toilet water.

Of the bacteria found in the ice, three out of the five restaurants tested positive for fecal coliform or E. coli, organisms that come from the feces of warm-blooded animals.

Health symptoms related to the presence of coliform include cramps and diarrhea. E. coli can cause intestinal illness and, in rare cases, hemolytic uremic syndrome, a serious kidney condition.”

Shudder…..

American Dietetics Association Promoting Ice Cream

The American Dietetic Association is still stuck with the idea that low-fat is healthier and is set to promote sweets on their website – in today’s “Tip for the Day” we don’t find suggestions about making delicious vegetables or tantalizing meals…nope, we find the association telling us how to include ice cream in our diet – and not just any ice cream, but specifically ice cream that is low in fat!

We All Scream for Ice Cream!
February 15, 2006
Ice cream is one of America’s favorite desserts. In today’s freezer sections you find many options for lower-fat brands. In a half-cup serving:

Reduced-fat (2 percent) ice cream has at least 25 percent less fat than regular ice cream.
Low-fat (1 percent) ice cream has three grams or less of fat.
Light ice cream has at least 50 percent less fat.
Fat-free ice cream has less than one-half gram of fat per serving.

Do you enjoy the creamy texture and flavor of premium ice cream, which has more fat and calories? If so, cut back on fat somewhere else in your eating plan so you can enjoy this treat, or eat a smaller portion than you normally would.
Produced by ADA’s Public Relations Team

Who is on their “Public Relations Team” and why are they promoting ice cream?

And how did they miss their obligation to the public as defined in the Code of Ethics for the Profession of Dietetics as published in the January 1999 Journal of The American Dietetic Association:

The dietetics practitioner practices dietetics based on scientific principles and current information.

We’re in the middle of an obesity epidemic and they’re promoting ice cream?

The dietetics practitioner is alert to situations that might cause a conflict of interest or have the appearance of a conflict. The dietetics practitioner provides full disclosure when a real or potential conflict of interest arises.

Did they “forget” to disclose that their organization receives money from companies that make ice cream?

Did they “forget” to mention that corporate sponsors get help from their organization in “telling a good nutrition story”?

The American Dietetic Association works with food companies and other organizations to develop materials and programs that deliver credible, science-based food, nutrition and health messages to consumers and to ADA members. If you have a good nutrition story to tell, ADA can help you tell it through collaborative and creative programs. These can include: custom nutrition education programs with consumer brochures and professional information materials; Web site interactive tools for consumer education; on-package nutrition messages; nutrition fact sheets; list rental for direct mail; advertising opportunities in the Journal of the American Dietetic Association and ADA Times; and sponsorship opportunities for meetings, continuing education teleconferences and Webinars.

While the American Dietetics Association wants to be the “most valued source of food and nutrition services,” their actions betray consumer confidence when they are promoting ice cream while we’re in the middle of an obesity epidemic!

Comparing Low-Carb to Low-Fat: Analyzing a review

The key to a quality meta-analysis rests in the quality of the studies included in the review. While the media continues to headline the recently published review of studies – Effects of Low-Carbohydrate vs Low-Fat Diets on Weight Loss and Cardiovascular Risk Factors – few are questioning the methods, analysis or conclusions.

As I pointed out yesterday, the researchers failed to include an important analysis in the paper – the change in cholesterol ratio (total cholesterol/HDL cholesterol) in their review. This is an important piece of information that is missing and must be part of the equation used to determine the efficacy of low-carb diets in the short and long-term.

More importantly though is the fact that the review failed to include only studies that actually met their inclusion criteria, stated in the full-text as “To be included in this meta-analysis, trials were required to use a randomized controlled design comparing the effects of a low-carbohydrate diet (defined as a diet allowing a maximum intake of 60 g of carbohydrates per day) without energy intake restriction vs a low-fat diet (defined as a diet allowing a maximum of 30% of the daily energy intake from fat) with energy intake restriction in individuals with a body mass index (calculated as weight in kilograms divided by the square of height in meters) of at least 25. Included trials had to report changes in body weight by using an intention-to-treat analysis, to have a follow-up of at least 6 months, and to include individuals 16 years and older. We excluded trials with crossover or sequential designs.”

In reviewing the studies that made the final cut, it’s apparent that not all met the inclusion criteria because some failed to implement the treatment as defined in the study in one or both groups.

Case in point – Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. JAMA. 2005;293:43-53. FULL TEXT – set out to compare four different dietary approaches with specific macronutrient restrictions:

• Atkins = 20g or less carbs per day, gradual increase to 50g per day
• Ornish = 10% fat per day vegetarian
• Weight Watchers = 24-32 “points” (1200-1600 calories) per day
• Zone = 30% fat, 40% carbohydrate, 30% protein

So far, so good – this trial did indeed look to compare low-carb and low-fat. But, did the groups actually follow the diets?

That is an important consideration when including a trial in a meta-analysis of comparable trials. And in this instance, this trial failed to maintain the inclusion criteria for the meta-analysis since participants across all groups in the study failed to eat according to their diet group requirements – they failed in “dietary adherance” of the trial – at all timed follow-ups in the study:

• Atkins
  1-Month = 68g carb (+18g to +48g of restriction goal)
  6-Month = 190g carb (+140g of restriction goal)
  12-Month = 190g (+140g of restriction goal)
• Weight Watchers
  1-Month = 1477 calories (within range)
  6-Month = 1755 calories (+155 calories of restriction goal)
  12-Month = 1832 calories (+232 calories of restriction goal)
• Zone
  1-Month = 45:32:23
  6-Month = 45:31:24
  12-Month = 40:36:24
• Ornish
  1-Month = 17% calories from fat (+7% of restriction goal)
  6-Month = 29% calories from fat (+19% of restriction goal)
  12-Month = 32% calories from fat (+22% of restriction goal)

Now while this study wanted to follow four different groups eating four different diets, the participants were not in compliance with their respective dietary restrictions. This study simply cannot provide us with usable data about how a low-carb diet (60g or less carbs per day) effects cholesterol when compared with a low-fat diet (30% or less calories from fat per day).

Of the six studies that “made the cut” for inclusion, we find that researchers were able to achieve participant compliance in only one study used for the meta-analysis. One other did not report the diet composition at baseline or during follow-up, so we have no way of knowing if those participants actually ate the assigned low-carb diet or low-fat diet.

When attempting a meta-analysis it’s important to not only find studies that meet your intial inclusion criteria, but to also assure that you’re comparing apples-to-apples data. This meta-analysis is not doing that and is therefore just another that attempts to do what is currently impossible – tell us if a low-carb diet (a truly low-carb diet) is better, the same or worse than a low-fat diet.

Did I just say “impossible”…?

Yes, I did.

Unfortunately we have no really good long-term studies comparing low-carb diets to anything else – low-fat, Mediterranean, standard American – nada, zip, zilch.

We need them. We need studies that don’t just set out to have subjects eat a low-carb diet and then don’t – we need those participating to actually stick to it so we can really see how a low-carb diet performs not only for weight loss, but also for reduction of risks and benefits to health.

I have to tell you though, until we move past the fat-phobia that is embedded in the collective thinking, this is going to be a difficult task – studies are compromised too often by those guiding the participants when they include advice on what to eat from dietitians who are committed to the concept that dietary fat and saturated fat is harmful, who are dedicated to the idea that restricting most fruits for a period is detrimental to health or hold that one must have grains in their diet for health.

It really isn’t all that hard to pick out those studies that sought to investigate the effects of a low-carb diet, yet stifled participants attempts with fat-phobic recommendations in the process. The quick way to tell if those following low-carb were given poor advice about dietary fats for a low-carb diet…ask – what amount of total fat and saturated fat did particpants eat?

If they were instucted to follow Atkins (or an Atkins-type low-carb diet) at minimum they’ll eat 60% of calories from total fat and about 15-18% of calories from saturated fat each day on 1600-calories. Cholesterol intake goes way up if one is following a low-carb diet according to the “rules” established by Dr. Atkins in his books.

Yet when we look at another study included, Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab. 2003;88:1617-1623. FULL TEXT – we find that part of the intervention included “Two registered dietitians delivered a 3-month intervention aimed at promoting dietary compliance. Group meetings with subjects on the same diet were held biweekly on the University of Cincinnati campus and addressed cooking tips, stress management, behavior modification, and relapse prevention. On alternating weeks, subjects met for individual counseling sessions during which their assigned dietitian reviewed their 3-d food records from the previous week, analyzed by Nutritionist V (First Data Bank, San Bruno, CA), and provided dietary recommendations and positive reinforcement. Subjects were advised to continue their baseline level of activity.”

With this potential to corrupt the dietary recommendations to the low-carb group – to basically cause them to eat a diet with less fat – let’s see how those participating in the low-carb arm ate at the follow-ups:

• 3-Month
  1156 Calories
  57% fat (71g fat)
  15% carb (41g carb)
  28% protein (78g protein)
  Cholesterol – 461mg
• 6-Month
  1302 Calories
  46% fat (65.5g fat)
  30% carb (97g carb)
  23% protein (74g protein)
  Cholesterol – 285mg

After years of designing menus to comply with the Atkins diet, the above ratios and gram-intakes are IMPOSSIBLE if one is just following the recommendations in Dr. Atkins’ New Diet Revolution. I can speculate what happened though – at the 3-month follow-up when the dietitians saw 461mg of cholesterol in the diet of those following low-carb, they panicked and started down the road of altering the diet to reduce the intake of cholesterol.

Want to know what happened?

From baseline to the 3-month mark, those following the low-carb diet saw their total cholesterol drop from 206 to 185, their LDL drop from 124 to 113, their HDL increase from 51 to 54 and their blood pressure drop from 116/79 to 112/72. All undeniably improvements in risk markers.

After changing their macronutrient intakes – specifically reducing their fat, saturated fat and cholesterol while increasing carbohydrate intake…those following the low-carb diet watched their total cholesterol rise from 185 to 205 (back to where they started), their LDL increase to 124 (where they started) and their HDL continue to rise to 58 (thankfully since this offset their other changes in cholesterol. In addition their blood pressure went up too – to 114/74.

We find such problems in a number of studies trying to investigate low-carb diets – those who are part of the intervention are interferring with what participants are eating because they’re entrenched in the belief that dietary fats and cholesterol are harmful and therefore unacceptable in the diet at any level above what is recommended.

Part of the process of discovery is to leave your assumptions behind and let those in a trial follow the study design without trying to adjust things that we “think” might be bad. Let the data come as it will – don’t interfere. As we can clearly see in the above, those who were allowed to eat high levels of fat and cholesterol were having some great improvements – when they altered that and changed how they were eating, they lost those improvements rapidly.

Low-carb diets hold so much promise – yet we can’t seem to grasp that study participants should just be allowed to follow the low-carb recommendations, which include eating higher amounts of cholesterol and dietary fat. Until we finally accept the idea of doing a study and allowing participants to eat freely from the foods allowed, we’re not going to answer the critical questions to determine the safety or efficacy of low-carb diets!

Low-Carb Diets Improve Cholesterol Ratios More than Low-Fat Diets

As usual, the media jumps to decalre that low-carb diets aren’t good for you:

• Dueling Diets: Low-Carb Equals Low-Fat for Weight Loss but Boosts Cholesterol
• Low carb diets help weight loss, but may raise cholesterol
• ‘No evidence’ low-carb diets are good for your heart
• Atkins diet hikes ‘bad’ cholesterol levels

The articles all try to disseminate the review published yesterday in the Archives of Internal Medicine, Effects of Low-Carbohydrate vs Low-Fat Diets on Weight Loss and Cardiovascular Risk Factors (Arch Intern Med. 2006;166:285-293), led by researchers from the University Hospital Basel, Switzerland.

The conclusions, from the abstract – Conclusions Low-carbohydrate, non–energy-restricted diets appear to be at least as effective as low-fat, energy-restricted diets in inducing weight loss for up to 1 year. However, potential favorable changes in triglyceride and high-density lipoprotein cholesterol values should be weighed against potential unfavorable changes in low-density lipoprotein cholesterol values when low-carbohydrate diets to induce weight loss are considered.

Later, in the discussion section of the full-text, we find the following ominous warning: In our opinion, the unfavorable changes in LDL-C levels caution against the conclusion that low-carbohydrate diets can be generally recommended to promote weight loss. No trials of low-carbohydrate diets have been performed that are powered for clinical end points (eg, myocardial infarction or death). It is therefore uncertain whether the beneficial effects of these diets on HDL-C and triglyceride levels outweigh the unfavorable changes in LDL-C level. In contrast, trials of reduced-fat diets, in conjunction with other lifestyle modifications such as increased physical activity, have demonstrated long-term maintenance of weight reduction and delayed onset of diabetes. Furthermore, randomized controlled trials have also demonstrated the benefits of the Mediterranean diet on secondary prevention of cardiovascular disease.

As I started to read through the paper, one thing was clear, the analysis was short-sighted and failed to include important additional information – namely the improvement or decline in cholesterol ratios, a standard used by clinicians to determine one’s risk of heart disease. There are two such ratio calculations that may be used – the TC/HDL ratio (total cholesterol to HDL) or the LDL/HDL ratio.

I’m not sure why the researchers failed to include this data, but it is quite revealing and should have been included. You’ll see why in a moment…first let’s look at the studies included:

• Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab. 2003;88:1617-1623.FULL TEXT
• Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med. 2003;348:2082-2090.FULL TEXT
• Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med. 2003;348:2074-2081.FULL TEXT
• Stern L, Iqbal N, Seshadri P, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med. 2004;140:778-785. FULL TEXT
• Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med. 2004;140:769-777.FULL TEXT
• Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. JAMA. 2005;293:43-53.FULL TEXT

To compare the data, they followed a very simple approach – actual numbers from baseline to six months or baseline to one-year and measured individually the changes in Total Cholesterol (TC), LDL, HDL and Triglycerides (TG). And quite frankly, when we review this simplistic analysis, things do indeed look bleak for the low-carb diet’s impact on cholesterol levels.

But what’s missing?

Ahhh…the baseline ratios compared with the follow-up ratios or TC to HDL! This is an important ratio to pay attention to – when a diet causes the ratio to decrease, that’s good – if it causes the ratio to increase, that’s bad. When comparing two dietary approaches, looking at the impact each has on the baseline ratio to the follow-up ratio is, in my opinion, a much better determinant of how the diet is increasing or decreasing risk of something like cardiovascular disease. And, I’m not alone with this thinking – in fact, studies support that “In addition to LDL cholesterol, the total to HDL cholesterol (TC/HDL) ratio is one of the most potent lipid predictors for cardiovascular disease.”

What do these ratios look like? How about we take a look now…

What does the data now tell us?

On average, at six-months, those following a low-carb diet improved (lowered) their TC/HDL ratio by 13% compared to the low-fat diet improvement of 6.6%. Add to this, those on low-carb averaged a 24.6% decrease in their triglycerides compared with the 6.8% decrease by those following low-fat – a more than three-fold improvement in the low-carb group.

On average, at one-year, those following a low-carb diet improved (lowered) their TC/HDL ratio by 7.6% compared to the low-fat diet improvement of 6.8%. Add to this, those on low-carb averaged a 19.6% decrease in triglycerides compared with a 7% decrease by those following low-fat – more than a two-fold improvement in the low-carb group.

What none of this data can tell you though is if the subjects actually ate a low-carb diet!

Unfortunately Foster et al doesn’t include macronutrient consumption in their paper, but all the other authors did. While the inclusion criteria in the present review stated that the data reviewed would meet this criteria: To be included in this meta-analysis, trials were required to use a randomized controlled design comparing the effects of a low-carbohydrate diet (defined as a diet allowing a maximum intake of 60 g of carbohydrates per day) without energy intake restriction vs a low-fat diet (defined as a diet allowing a maximum of 30% of the daily energy intake from fat) with energy intake restriction in individuals with a body mass index (calculated as weight in kilograms divided by the square of height in meters) of at least 25.

We find instead that the stubjects in the studies were actually eating more carbohydrate:

At the six month follow-up, subjects following “low-carb” were consuming:

• Samaha 150.7g carb 37.8% of calories
• Yancy 29.5g carb 8.0% of calories
• Dansinger 190.0g carb 41.1% of calories
• Brehm 98.6g carb 39.7% of calories

At the one-year follow-up, subjects following “low-carb” were consuming:

• Stern 120.0g carb 32.8% of calories
• Dansinger 190.0g carb 40.2% of calories

Once we begin to really look at this data, we now understand that with the exception of one (maybe two if subjects in Foster et al consumed less than 60g of carbohydrate each day) that this review isn’t really a meta-analysis of low-carb diets versus low-fat diets, but controlled-carb diets versus low-fat diets.

This is an important distinction since the evidence thus far tells us that strictly controlling carbohydrate – to truly “low-carb” levels of 60g or less of carbohydrate a day – does have an even greater capacity to improve TC/HDL ratios and triglycerides.Generally, it is understood within the scientific community that low-carb diets must be no more than 60g of carbohydrate a day to be deemed “low-carb” and that higher intakes of carbohydrate that remain at or below 40% of energy from carbohydrate are not “low-carb” but “controlled-carb” or “carbohydrate restricted.”

The researchers of this particular paper failed to note the carbohydrate level consumed or its potential relation to cholesterol outcomes.

They also failed to really do the important work of examining whether these controlled-carb diets improved overall TC/HDL ratios. As we see above, they did and much more so than the low-fat diets.

When we take the overall improvements in TC/HDL ratios and also look at improvements in triglycerides, who can say with a straight face that controlled-carb isn’t a better better approach?

Low-Fat Diets – Dogma or Data?

Main Entry: dog·ma
Function: noun
Etymology: Latin dogmat-, dogma, from Greek, from dokein to seem
1 a : something held as an established opinion; especially : a definite authoritative tenet
b : a code of such tenets
c : a point of view or tenet put forth as authoritative without adequate grounds

Main Entry: scientific method
Function: noun
1. the principles and empirical processes of discovery and demonstration that are characteristic of or necessary for scientific investigation.

The scientific method involves an observation, the formulation of a hypothesis about the observation, experimentation designed to demonstrate the truth or falseness of the hypothesis, and a conclusion that validates or modifies the hypothesis.

As I’ve pointed out a number of times, dogma isn’t science.

Science is an objective, disciplined methodology for investigating the world around us. Scientists — those having expert knowledge of one or more of the existing scientific disciplines – use the scientific method in their efforts to extend and deepen our understanding of the world. Good scientists are open the prospect of being humbled by their findings. You see, scientific inquiry isn’t about being “right,” it’s about finding truth through a mindset of doubting, questioning, and openness to the self-correcting spirit of scientific inquiry.

The necessary commitments of a scientist in search of the truth include:

• A search for collectively justified knowledge (as opposed to opinions and unjustified beliefs)
• A justification based on perceptual grounds not shaped by individual or cultural factors
• A willingness to change if required by evidence and reasoning (open-mindedness)
• An unwillingness to change unless required by evidence and reasoning (skepticism)
• An awareness of the fallibility of human knowledge, and the resultant doubting and questioning

Interestingly, the words “science” and “scissors” are both related to the Greek word “schizo” meaning “to split.”

Think of science as scissors: two blades of inquiry are better than one for cutting into the unknown.

Today explanations of WHI findings are being interpreted, refined and subsequently targeted to the consumer through a biased filter, with the actual data judged right or wrong depending on whether or not it supports the low-fat dogma. Discordant data on carbohydrate restriction, saturated fat intake, and metabolic syndrome, among other topics, continue to be ignored or ridiculed.

This reflects a continued mindset that is alien to the spirit of free scientific inquiry.

Just take a look at the headlines and commentary that is pervasive in the media right now:

NEWSWEEK: Dean Ornish: The Facts About Fat
The real lesson of the Women’s Health Initiative study is this: if you don’t change much, you don’t improve much.

TIME: The Real Story About Low Fat
What does all this mean for you? If you don’t have a history of heart disease or breast or colon cancer, you can probably cut yourself a little slack on the total amount of fat you consume–as long as you avoid the bad fats (found, for example, in ice cream and ground beef) and replace them with good fats (found in olive oil, nuts and fish). We should all exercise regularly and eat more fruits, vegetables and fiber-rich whole grains. And next time someone says to you, “Hey, wasn’t there a study that proved that low-fat diets aren’t worth it?”, you can just smile and ask that person to pass the string beans.

NEWSWEEK: The New Fight Over Fat
This study did not repeal the laws of diet as much as it refined them. It did not, repeat not, say that whole grains, fruits and vegetables can be tossed out in favor of thickly marbled beef at every meal.

CHICAGO TRIBUNE: Fat free? Not really
Even after this definitive study, though, most nutritionists (except for those in the Atkins ultra-low-carb camp) still think there’s a benefit to limiting fat consumption.

NUTRAINGREDIENTS: The cost of bad research
Some experts have rightly spoken out against the studies, encouraging the public to stick with five portions of fruit and vegetables a day and stressing that people take care about fat intake…There will undoubtedly be consumers who accept these studies, people who are reluctant to change their diet or lifestyle, despite a mountain of science saying the opposite.

BUSINESS WEEK: Skip Your Veggies? Not So Fast
Based on its design, the trial had little chance of making major advances in the science of nutrition…So try to stay fit, keep your weight down, aim for a relatively healthy diet, and don’t worry too much about the latest headlines in the medical journals.

US NEWS & WORLD REPORT: A low-fat diet, by itself, won’t arm you against heart disease or colon cancer
Moreover, the recommended diet made no distinction between “good” unsaturated fats and “bad”saturated fats and trans fats, whose importance to heart health has been recognized since the data-gathering started. And since all the women in the study were eating fairly healthfully beforehand, it’s possible that the small changes in vegetable and grain consumption by the dieting group weren’t big enough that any benefits registered. Rather than focus on total fat intake, Stefanick advises, go easy on foods containing saturated fats and trans fats and eat more vegetables and fruits and whole grains.

FASHION MONITOR: Low Fat Diet Study Results Don’t Prove Much, Dieticians Say
Despite findings being announced this week that a low-fat diet introduced in the middle-age years didn’t reduce the risk of breast cancer, heart disease, stroke or colon cancer, one of the researchers says people still need to focus on the types of fat they eat.

GLOBE AND MAIL: Ignore the latest study stay on a low-fat track
But just because this one study didn’t find an overall protective effect, there’s no reason to swap a low-fat menu for one that’s high in fat.

Giving support only to beliefs within the framework of a low-fat diet undermines a fundamental element of the scientific method — the constant testing of theory against observation. Such a restriction makes objective, or even the ideal – unbiased, discussion and research impossible.

So what is the scientific community about, really? To what extent are scientific theories defined by the quest, not for truth, but for job security and lavish government funding? Let’s not forget the WHI study cost almost a half-billion dollars and now researchers want more time and a stab at observing the consequence of restricting dietary fat even more, and in the meantime, the low-fat dogma will remain as the dietary approach for all Americans.

Remember it was the Director of the National Heart, Lung, and Blood Institute (NHLBI), Elizabeth G. Nabel, who said – “The results of this study do not change established recommendations on disease prevention. Women should continue to get regular mammograms and screenings for colorectal cancer, and work with their doctors to reduce their risks for heart disease including following a diet low in saturated fat, trans fat and cholesterol.”

Where is the principle of scientific humility? You know that piece that is integral to science – our admission to our express lack of knowledge about everything.

What’s missing in all the discourse is the reality that accumulative error certainly does apply when theories are built on theories that are built on theories that are only assumed to be true. The scientific community has a way of constructing systems of “knowledge” despite dissent at multiple points along the way. For decades there has been dissent from numerous scientists who warn that a low-fat diet is not optimal. This dissent hasn’t been quieted by evidence and hard-data, but by ridicule and dismissal.

But, we laypersons rarely hear of the dissent — only the prevailing view prevails precisely because dissent and evidence is ignored. And we’re seeing this now.

An empirically derived worldview is held as a matter of evidence, not faith that what you think is right is right; it’s responsive to observation of a world that’s understood to exist independently of the needs and desires that dogma so often flatters.

Empiricism therefore keeps us cognitively humble.

Implicit in the cognitive norms of empirical evidence and observation is the assumption of fallibility, the idea that we may not be getting everything quite right, that we might someday have a more accurate view of reality based on more reliable and comprehensive observations and evidence. We’re seeing no sign that those committed to the low-fat dogma even consider they might have a flawed hypothesis.

This fallibilism helps to inoculate evidence-based science against the self-righteousness of being necessarily right. Those scientists committed to unfettered inquiry are unlikely to resort to threats and coercion to silence opposing views.

In contrast, we find adherents of dogmatic views of reality are unresponsive to evidence and are less inclined toward cognitive humility. Their driving assumption can be quite the opposite of fallibilism and reads like this: my revealed, intuited, empirically non-responsive worldview is necessarily true, so any contradictions of it must be discounted as illusory and wrong-headed. Since I am right, others must be wrong, and their beliefs stand as an insult to my truth.

In his famous 1974 commencement address at Caltech, Richard Feynman provided an inspiring example of how science ought to be practiced. He began by warning against self-deception, the original sin of science, saying that “The first principle is that you must not fool yourself, and you are the easiest person to fool.”

To avoid self- deception scientists must bend over backwards to report data that casts doubt on their theories. Feynman applied this principle specifically to scientists who talk to the public: “I would like to add something that’s not essential to the science, but something I kind of believe, which is that you should not fool the laymen when you’re talking as a scientist. . . . I’m talking about a specific, extra type of integrity that is not lying, but bending over backwards to show how you’re maybe wrong, [an integrity] that you ought to have when acting as a scientist. And this is our responsibility as scientists, certainly to other scientists, and I think to laymen.”

That’s such an incredible statement – Feynman’s kind of science has the virtue of humility at its very core. Honesty and humility.

This is what has to be brought into the national obesession with dietary fat – an understanding of the obligation of science to separate personal belief & dogma from scientific investigation, to maintain that separation and be honest about it, and not to mislead the public about what has been demonstrated and what hasn’t; a science that sticks to its data, that is careful to consider alternative explanations, and that does not allow itself to be ruled by a dogmatic agenda of any kind; a science that does not commit the original sin of believing what you want to believe.

A science in which the scientists do not fool themselves and therefore do not try to fool the public either.

Separating empirical science from dogma is a big job, and everyone with the right spirit can contribute to it. If you are a scientist, you can follow the path set by thought-leaders and those history shows were once persecuted yet eventually prevailed, to bring out the crucial information that is not widely reported because it does not fit preconceptions. You can encourage your colleagues to speak out against those who abuse their authority by using it to promote dubious recommendations as if they had been empirically confirmed.

We need people who have enough courage to say this to the low-fat dogmatists: “We’re going to challenge the claims that you’re making that seem to go beyond what you know.”

We need to have lots of people doing just that.

What we need now is people who want to get thinking going in the right direction, not people who think they have all the answers in advance.

If we get an objective scientific process started, we can have confidence that it will bring us closer to the truth. Those preaching the low-fat dogma rely on confining their critics in a stereotype. They have learned to keep their own philosophy on the stage with no rivals allowed, and now they have to rely almost exclusively on maintaining the low-fat dogma in the cultural mindset.

The current low-fat dogma is like a great battleship afloat on the seas of evidence-based reality. The ship’s sides are heavily armored with barriers to criticism, and its decks are stacked with rhetorical guns to intimidate would-be attackers. In appearance, it is impregnable – but the ship has sprung a evidence leak, and that leak widens as more and more people understand it and draw attention to the conflict between empirical science and dogma driven consensus.

The most perceptive of the ship’s officers know that the ship is doomed if the leak cannot be plugged and they scramble to innundate the media with pleas to ignore the findings and data that cripple the ship. The struggle to save the ship will go on for a while, and there will even be academic rearranging of the chairs on the deck by those committed to the low-fat dogma as they remain confident the ship will not sink. In the end, the ship’s great firepower and armor will only help drag it to the bottom. Reality will win.

Reality will win because the data speaks volumes.

Just Give Us More Time….Pretty Please….

On the heels of the “null findings” of Women’s Health Initiative Dietary Modification Trial for reduction of risk in breast cancer and cardiovascular disease, we’re seeing a call for continued follow-up and more rigorous restrcition of dietary fat to prove a low-fat diet offers some protection to health.

Have we lost our minds?

The biggest study so far investigating the relation between breast cancer and fat intake is the Nurses’ Health Study, conducted by Harvard University Medical School. A total of 88,795 women free of cancer in 1980 were followed up for 14 years. Comparing breast cancer rates in women who derived more than thirty percent of their calorie intake from fat with women who derived less than twenty percent of calories from fat, they show that those on low-fat diets had a higher rate of breast cancer than those who ate more total fat.

Dr Michelle Holmes and colleagues concluded: “We found no evidence that lower intake of total fat or specific major types of fat was associated with a decreased risk of breast cancer.”

Yet the researchers for the WHI trial want more time? To show what – a trend toward a higher incidence of breast cancer in the women eating low-fat diets?

In 1997 the Nurses’ Heath Study (noted above) researchers found that “Total fat intake was not signficantly related to the risk of coronary disease.”

In 1997 it was found that low-fat, high-carbohydrate diets [15% protein, 60% carbohydrate, 25% fat] increase the risk of heart disease in post-menopausal women. The researchers were clear in their conclusion that a low-fat diet “would increase risk of ischemic heart disease in postmenopausal women,” and that “it seems reasonable to question the wisdom of recommending that postmenopausal women consume low-fat, high-carbohydrate diets.”

Dr. Gerald M. Reaven, of Stanford University School of Medicine in California, and colleagues compared the effects of a low-fat, high-carbohydrate diet [25% fat, 60% carb, 15% protein] with a high-fat, lower-carbohydrate diet [45% fat, 40% carb, 15% protein], on blood fats and cholesterol. They found their subjects had significantly higher fasting plasma triglyceride concentrations, remnant lipoprotein cholesterol concentrations, and remnant triglyceride concentrations when they were on the high-carbohydrate, low-fat diet, both after fasting and after breakfast and lunch. The study participants also had significantly lower HDL (the ‘good’ cholesterol) concentrations on this diet.

The authors conclude: “Given the atherogenic potential of these changes in lipoprotein metabolism, it seems appropriate to question the wisdom of recommending that all Americans should replace dietary saturated fat with CHO [carbohydrate].”

In 2004, researchers concluded that “In postmenopausal women with relatively low total fat intake, a greater saturated fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression.” The women followed were consuming an average of 25% total fat – lower than the women in the WHI trial.

Yet the researchers for the WHI trial want more time? To show what – a trend toward a higher incidence of cardiovascular disease in the women eating low-fat diets?

Blast from the Past

While the media and experts continue to spin their wheels in an effort to save the low-fat diet from demise, I’d like to travel back today, to 1971 to review a study conducted before Dr. Robert C. Atkins published Dr. Atkins’ Diet Revolution (which was later revised and published as Dr. Atkins’ New Diet Revolution).

I hadn’t known about this study until this week – and wow, it’s an eye-opener! It paints a very clear picture that we’ve known for decades just how effective a low-carb diet is, but have been fed a steady diet of low-fat lies as our nation has grown overweight and obese over the last three decades.

The study, Effect of body composition and other parameters in obese young men of carbohydrate level of reduction diet, was published in the American Journal of Clinical Nutrition in March of 1971. It was designed to investigate the weight loss effect of diet with varying carbohydrate content and specifically kept protein intake and calories the same in those following the diets. By today’s standards for study design, this one is good since it controlled both calories and protein intake to have an accurate measure of how carbohydrate influenced weight loss, if at all.

The limitation, which must be stated up front, is that this was a small study on just eight collage aged men.

For three weeks they were fed a “maintenance diet” of, get this, 3000-calories a day, with 115g of protein, 425g of carbohydrate and 160g of fat (macronutrient percents – protein 12.8%, carbohydrate 47.2%, fat 40% – fairly close to the “norm” in 1971). Once this maintenance period ended, three groups consumed differing amounts of carbohydrate (and of course, fat). The diet compositions of each group, each consuming 1800-calories per day, were:

• Group A = 115g protein (25.5%), 104g carb (23.1%), 51.4g fat (51.4%)
• Group B = 115g protein (25.6%), 60g carb (13.3%), 122g fat (61.1%)
• Group C = 115g protein (25.5%), 30g carb (6.7%), 135.5g fat (67.8%)

With each group having a similar 3000-calorie a day maintenance requirement, then reduced to 1800-calories a day, or a calorie restriction of 1200-calories a day, who lost more weight?

For those committed to the calorie theory – that is “calories in = calories out” all three groups should have had similar weight loss, no?

Let’s see what happened…

• Group A lost 11.5kg (25.3 pounds)
• Group B lost 12.78kg (28.11 pounds)
• Group C lost 16.18kg (35.6 pounds)

Are you scratching your head yet?

Wait a minute, you may be tempted to say….that’s not possible!

The researchers added another nugget in the paper – they didn’t control for energy expenditure and when they calculated this, it seems that Group A had increased their energy use to 3400-calories a day, Group B upped theirs to just 3300-calories a day, and Group C used 3,400-calories a day.

Based on this additional piece of data, how much should each group have lost?

This is easy to figure out – they ate 1800 calories a day and burned either 3,300 or 3,400 per day, making a calorie deficit of 1500-1600 calories a day. They did this over 9-weeks, so their total deficit was 63 days x 1500-1600 calories a day = 94,500 or 100,800 calories, then divided by 3,500 calories that is a pound of weight loss = 27-pounds or 28.8 pounds.

• Group A should have lost 28.8-pounds and lost 25.3-pounds
• Group B should have lost 27-pounds and lost 28.11-pounds
• Groups C should have lost 28.8-pounds and lost 35.6-pounds

The researchers were intrigued and did something important – they measured how much of that weight loss was fat. And, this is where things get more interesting…

• Group A – 75% of their weight loss was fat
• Group B – 84% of their weight loss was fat
• Group C – 95% of their weight loss was fat

Still with me?

In the discussion section of the paper, the researchers basically concluded that “no adequate explanation can be offered” as to why weight loss and fat loss differed so dramatically between the groups. They continued that even after accounting for energy expenditure differences, that didn’t explain the differences seen in weight loss.

The researchers remarked in their conclusions that “Weight loss, fat loss, and percent of weight loss as fat appeared to be inversely related to the level of carbohydrate in the isocaloric, isoprotein diets. No adequate explanation can be given for weight loss differences.”

Here we are, some 35-years later – as a nation fatter than ever before – and still listening to the ‘experts’ tell us that carbohydrate restricted diets offer no benefit for weight loss and that restricting fat in our diets is the way to lose weight.

We have a very clear picture of what a calorie restricted, low-fat diet does after seven years – nothing! The WHI Dietary Modification Trial shows this – after seven years on a low-fat diet, the women eating a low-fat (and lower calorie) diet remained overweight at the end of the seven years, losing only about two pounds! Incidentally, this trial was touted as “proof” that low-fat diets don’t make you fat! How can anyone miss that this diet kept these women fat?

It’s time we – the average, everyday consumers – stand up and say “enough!” to those preaching the low-fat dogma that has no support from the evidence!

In all the years I’ve spent reviewing the data, I’ve yet to find just one study that compared a low-carb diet with a low-fat diet that showed better – or healthier – weight loss from a low-fat diet! In fact, every last study I’ve seen shows – clearly – that a low-carb diet is superior to a low-fat diet for weight loss and more importantly, loss of body fat.

So, are you tired of the low-fat lies yet?