Archive for October, 2006
You’ve gotta love it when research findings contrary to the conventional wisdom don’t do much to change the status quo or even challenge the assumptions we hold. Take for instance our belief that fruit is important in our diet and must be eaten each day to make sure we’re eating a healthy-balanced diet.
True? Probably not.
The data from various studies have shown many times that long-term health is not dependent upon eating fruit, nor any specific quantity of fruit each day. Yet, that hasn’t stopped the leading health organizations and government policy makers from repeatedly telling us to eat fruit, warning that diets that limit or restrict fruit are bad, and that we all need at least 2-3 servings a day or we’re going to have health problems.
Now don’t get me wrong – fruit is good, I like it, I eat it too; but it’s just not essential for our long-term health; especially if we’re eating a nutrient-rich diet and including non-starchy vegetables.
The latest study to explore the necessity of fruit in the diet was published in the October 24 issue of Neurology – Associations of vegetable and fruit consumption with age-related cognitive change – to investigate the role fuits and vegetables in the diet had for protecting against cognitive decline as we age. Just as the Nurses’ Health Study data showed previously, fruit consumption was not associated with a slower rate of cognitive decline, but vegetables, specifically non-starchy vegetables, were protective!
As reported by CBC News – the study “found that high consumption of fruit had no effect on thinking ability.”The lead researcher, Dr. Martha Clare Morris, said “By far, the association with a slower rate of decline was found in the group that ate high amounts of green, leafy vegetables.” Such foods included lettuce and tossed salad, spinach, kale and collards. The study also found that the slowdown in cognitive decline was greatest in the oldest people who ate at least two more vegetable servings a day.
Take home message here – eat your vegetables, specifically non-starchy vegetables.
So far as fruit – it’s fine to include in your diet if you want to, I just don’t think you must include fruit to be healthy; it’s a nice, sweet addition that also packs in antioxidants; but there doesn’t appear to be any big benefit long-term to eating fruit every day.
Interestingly, some countries with better health and longevity actually eat less fruit each day than we do in the United States. So next time you hear about how miserable our intake of fruit is in the US, remember too that Japan, France, Iceland, Switzerland and others eat less fruit than we already do and they live longer and in better health too. Keep in mind they each, also, eat a lot more non-starchy vegetables each day!
Yahoo! News recently carried a press release about a study published from researchers in the Neatherlands; their finding – subjects with diabetes glow in the dark. The researchers investigated the use of a new non-invasive tool to determine if it could accurately detect skin florescence due to the accumulation of AGEs (advanced glycosylation end products) in the skin of those with diabetes. AGEs are produced in the body when glucose binds with proteins – as they build up, they damage blood vessels and cause complications such as nerve and vascular damage.
From previous studies (Dec 2005; June 2005; July 2004) the researchers knew these AGEs have florescent properties, and this study “confirmed that those properties could be measured by illuminating the skin, and that high levels of autofluorescence were associated with more severe diabetes complications, such as neuropathy, retinopathy and cardiovascular problems.”
The lead researcher, Dr. Helen Lutgers, said of the finding, “With this tool, doctors could easily check people with diabetes in an outpatient clinic setting to see whether they may already be developing dangerous complications. The sooner complications are detected, the better the chance of preventing progression of damage.”
Here’s the rub – while the device used in the study, DiagnOptics AGE-Reader, is available commercially in Europe and is being used by doctors there, it isn’t available to healthcare professionals here in the US because it is “restricted to experimental use only,” as it awaits FDA approval.
How insane is that? A non-invasive device – shine a light and then in 30-seconds have a result that offers a good measure of accumulated AGEs in the skin by the elbow – that can’t get past the FDA approval process?
This is some pretty cool technology if you ask me. It’s non-invasive, quick and from the data thus far, reliable and accurate. Considering the very damaging complications from diabetes, especially from AGEs, use of this type of device should be “standard of care” for those with diabetes. I’d even go so far as saying it would be a great add-on in the “standard of care” for any doctor’s office visit since the test is quick and simple and the result could prompt further testing to see if someone who has a high measure of florescence has undiagnosed diabetes and is already suffering with complications even though they don’t know it!
Jimmy Moore, the author of Livin’ La Vida Low Carb blog and book has hit the airwaves with his own show – the Livin’ La Vida Low-Carb Show. He once weighed over 400 pounds, then lost over 180 of those pounds following a low-carb diet and has never looked back.
The new weekly podcast is hosted by Grasshopper New Media and new episodes are broadcast each Monday. His strongest belief is that the power to change is in your hands and he hopes the podcasts will inspire.
If you’re trying to lose weight – how you do it is up to you. His experience is there to help you “Just do it.”
Take a moment and drop on over and check out his new show.
Chalk up another important study the media isn’t talking about…The November issue of Diabetes Care published Trends in Hyperinsulinemia Among Nondiabetic Adults in the U.S. which found the mean fasting insulin of non-diabetic adults rose approximately 5% from the NHANES III survey in 1988-1994 to NHANES 1999-2000.
The researchers concluded in the abstract “In parallel with the obesity epidemic, concentrations of fasting insulin and prevalence of hyperinsulinemia have increased remarkably among nondiabetic U.S. adults.”
As the researchers noted, focusing on fasting hyperinsulinemia has two advantages:
- it is as good a surrogate estimate of insulin resistance as are various combinations of fasting insulin and glucose concentration such as homeostasis model assessment or quantitative insulin sensitivity check index.
- of greater clinical relevance is the pathophysiological role that hyperinsulinemia plays in the development of the abnormalities and clinical syndromes that occur more commonly in insulin-resistant subjects. Thus, quantifying the changes in fasting insulin concentration over time provides information regarding both the increasing prevalence of insulin resistance and the potential clinical consequences of this phenomenon.
Put simply – we have a problem in the United States; if it is not reversed it will mean a higher incidence of chronic degenerative disease in our population in years to come.
The researchers provide a laundry list of what hyperinsulemia and insulin resistance is associated with in terms of health outcomes “increased risk of type 2 diabetes, coronary heart disease, essential hypertension, congestive heart failure, polycystic ovarian disease, nonalcoholic fatty liver disease, and cancers of certain sites such as prostate, colon and rectum, and breast.
These chronic diseases are major causes of death in the U.S. and other regions in the world. Furthermore, the burden of these chronic diseases has been growing in the U.S. and worldwide. Rapidly increasing trends in insulin resistance and compensatory hyperinsulinemia, if not properly controlled or altered, may predict adverse future courses of many health conditions that are linked to insulin resistance.”
I would have liked to see a more thorough discussion in the full-text about the changes that have occured concurrently with these findings, but the researchers only noted that “[t]he alarming increase in hyperinsulinemia, particularly among groups with a lower prevalence of insulin resistance, such as young adults and non-Hispanic white women, underscores the urgent need to address the root causes.”
No surprise the assumption remains that the population is getting fatter because we eat too much and exercise too little – “Because the major contributing causes of insulin resistance, such as obesity, poor dietary intake, and inadequate physical activity, are modifiable, clinical consultation and public health campaigns aimed to improve these health behaviors are needed.”
As I’ve noted previously, it’s more than just the calories that are causing our increasing waistlines, alarming rates of diabetes and other diseases, and continued decline in overall health. Until we address what is causing the alarming increase in hyperinsulinemia we’re not going to solve the problem.
To be sure, the problem is our diet, but it’s not the usual suspects – it’s not the calories and it’s not the saturated fat. It’s what we’re avoiding in our diet these days!
The researchers allude to the assumption that it’s simply a matter of eating properly, but this completely ignores the fact that a higher increase in the prevalence of hyperinsulinemia was found in men, who the data show, ate less calories in 2000 than they did in 1994 (2618 vs 2666). Not only that, but the 2000 data also showed men ate less fat as both a percentage of calories (33.9% vs 32.1%) and in absolute grams (100g vs 93g); less saturated fat as both a percentage of calories (11.3% vs 10.8%) and in absolute grams (33.5g vs 31.5g); and ate a similar intake of carbohydrate (321.25g vs 320.7g) and slightly less protein (102.6g vs 97.5g).
The fact is, in the NHANES 1999-2000 men ate closer to the dietary recommendations than at any previous period surveyed, yet the prevalence of hyperinsulinemia increased more in men than women (38.3% vs 32.1%) while their diet was supposedly improving. Add to this, even with the slight decrease in calories, the men also got fatter – something explained by a chronic state of hyperinsulinemia and insulin resistance.
In 2002, according to the World Health Organization (WHO) data, 72.2% of adult men (age 15+) in the United States had a BMI greater than 25.
So what’s going on?
I’ve said it before, and I’ll say it again – our focus on macronutrients as a percentage of our diet is wrong; our obsession with reducing saturated fat is wrong; and our unwillingness to let the data really tell us what is wrong is going to be our undoing.
Folks, the answer is right in the data itself – if only the researchers would step back and look at it without preconceived assumptions about what we should eat, they’d be able to see the glaring and obvious changes we’ve made in our diet since at least 1970 that are making us fat and sick.
We’re eating too much sugar, too many refined carbohydrates and not nearly enough quality protein.
Ahhh, yes, protein.
I write a lot about protein, don’t I?
The reason is that it’s not just protein per se that we require, but specific amino acids from foods rich with protein. In fact, the very foods we are told to limit and/or avoid in our diet – eggs, beef, lamb, whole milk and dairy products made from whole milk. We’re repeatedly told these foods have too much saturated fat and cholesterol – that we can get our protein from other foods, plant based foods, just as easily.
What we’re not told is the additional cost of calories to actually consume enough amino acids, in the amounts we require for those considered “essential,” if we’re eating plant-based proteins instead of animal based proteins!
For example, two eggs will cost you 142 calories and provide 12.5g of complete protein, that is it has the correct amount of essential amino acids for each gram of protein consumed.
Want the same 12.5g of protein from a plant-based source?
A slice of whole wheat bread costs you 75-calories and provides 3.1g of protein. It’s also not a complete source of protein since it has a limited amino acid – an amino acid that isn’t high enough to provide enough to complete the ratio needed for “complete” protein. So, you need to add another food with that limited amino acid, like peanut butter. So then, two tablespoons of peanut butter will cost you another 188-calories and provide 8.03g of protein. It too is a limited protein – lacking enough of a different amino acid than the bread, but together they work to provide enough of the amino acids needed. But, also important here – combined they also cost you 263-calories for that 11.3g of protein.
You’ve now eaten more calories and less protein – 121-calories more, 1g less protein.
Hey, you have eaten less saturated fat and cholesterol – but more carbohydrate, which means you need more insulin to lower your blood sugars as they rise with more carbohydrate.
And, still the researchers are trying to understand why there is an increase in hyperinsulinemia in the adult population? Why we’re getting fatter by the year? Why we’re seeing more diabetes and complications of high blood sugars and insulin?
Good grief – it’s right there is the data!
Our overall diet is WRONG for our metabolism, courtesy of the dietary guidelines of the last thirty years that have persisted in telling us to limit animal foods, eat more plant-based foods and limit cholesterol and saturated fat.
We need to re-appreciate the role of protein in our daily diet – specifically complete protein sources. Until we do we’re going to continue to see alarming increases in obesity, insulin resistance, hyperinsulinemia, and diabetes; and watch as our children are afflicted younger and younger.
We are simply not designed to eat the diet recommended; and now, after thirty odd years those recommendations are haunting us – mocking us as we reach for yet another bean burrito or whole grain cereal and skim milk in the mistaken belief it’s all about calories in and calories out, making sure we don’t eat too much saturated fat and choose more plant-based foods.
Like the canaries in the mine, slowly dying in the presence of odorless but harmful gases, we’re slowly dying in the presence of seemingly logical yet harmful dietary recommendations. All the researchers can keep repeating is eat less and move more; while encoraging us to eat more more whole grains, more fruits and vegetables, more skim milk and non-fat dairy, more beans, more soy and limit saturated fat by eating less meat.
Millions of Americans are consciously trying to lose weight and eat a better diet – the data tells us they are indeed trying to and succeeding in reducing fat and calories; it also tells us that in the process of doing this, they’re eating less protein and along the way, choosing incomplete sources of protein, thus they’re slowly bankrupting their health and well-being for the long-term.
Let’s not forget, the more you weigh, the more protein you require each day. So before you jump in with both feet to a diet that restricts your calories and is based on the dietary guidelines – remember this – doing so is going to significantly reduce your protein intake.
Just do the math.
If you weigh 250-pounds, you require (as per the IOM dietary reference intakes) a minimum of 90.9g of complete protein each day. Let’s say you’re eating 2,500-calories a day with 16% of those calories from protein – then you’re eating about 100g of protein each day right now – pretty darn close to what you require each day and most likely just about right when you consider you’re eating protein from many different sources, both complete and limited.
Go on a diet based on the recommendation for 1800-calories a day, with 30% fat, 55% carbohydrate and 15% protein, your protein intake just dropped to 67.5g a day – inadequate according to the IOM requirements for protein intake – in fact, you’ll be missing your protein requirement by 26% each day.
Now consider this – until you reach a body weight of 185-pounds (lose 65-pounds) that level of protein intake will continue to be chronically inadequate – all the while forcing your metabolism to work with less than it requires each day. We’re not talking calories here – we’re talking about the protein – the basic building blocks of every cell in your body and enzymes, hormones, immunoglobulins, neurotransmitters, nutrient transport and storage compounds and cell membrane receptors. How long do you really think your body will want to try to function at such a significant metabolic disadvantage?
And researchers are stumped as to why we’re growing fatter and sicker?
It’s right there, staring us in the face, in the data.
Eat your protein!
I’ll be away at the annual ASRM conference in New Orleans, and won’t be posting again, most likely, until next Thursday, October 26, 2006! Hope to have you back again soon!
Well, if you need more incentive to consider why it’s important to know where your food comes from – consider this:
Three years after the Food and Drug Administration first hinted that it might permit the sale of milk and meat from cloned animals, prompting public reactions that ranged from curiosity to disgust, the agency is poised to endorse marketing of the mass-produced animals for public consumption.
The decision, expected by the end of this year, is based largely on new data indicating that milk and meat from cloned livestock and their offspring pose no unique risks to consumers.”Our evaluation is that the food from cloned animals is as safe as the food we eat every day,” said Stephen F. Sundlof, the FDA’s chief of veterinary medicine, who has overseen the long-stalled risk assessment.
Farmers and companies that have been growing cloned barnyard animals from single cells in anticipation of a lucrative market say cloning will bring consumers a level of consistency and quality impossible to attain with conventional breeding, making perfectly marbled beef and reliably lean and tasty pork the norm on grocery shelves.
Where do I even start with this one, published in the October 3 issue of Nutrition? Low-carbohydrate and high-fat intake among adult patients with poorly controlled type 2 diabetes mellitus. (abstract)
It’s not really as study per se, but the findings of baseline dietary habits of subjects about to start a trial to investigate dietary intervention to control type II diabetes.
What caught my attention was the conclusion in the abstract, “This dietary pattern may represent a popular trend that extends beyond our particular study and, if so, has serious cardiovascular implications in this vulnerable population of T2DM patients.”
What, pray tell, is the dietary pattern in question?
Well, if we rely on publication title and what the researchers tell us, it is a low-carbohydrate diet; not only that, it’s this low-carbohydrate dietary pattern reported that is leading the way to cardiovascular complications down the road.
Abstracts like this one should have a warning: Beware, you’re about to enter the assumption-spin zone!
You know me….never quite content with the abstract alone, I want to see the data!
How about we take a look?
Before I go through the data reported in the study, how about I first review the ADA’s definition of what level of carbohydrate intake they consider a low-carbohydrate diet. You’ll see in a moment why this definition is important.
From the latest update to the ADA position statement: Nutrition Recommendations and Interventions for Diabetes–2006:
Twice they state the minimum carbohydrate intake levels to consume. First in the energy balance section with “Low-carbohydrate diets (restricting total carbohydrate to less than 130 g/day) are not recommended in the treatment of overweight/obesity;” and again in the nutrition recommendations section with “Low-carbohydrate diets, restricting total carbohydrate to less than 130 g/day, are not recommended in the management of diabetes.”
Even before they updated the Standards of Care this summer, their position statement published in January, Standards of Medical Care in Diabetes – 2006, stated “Low-carbohydrate diets (restricting total carbohydrate to less than 130 g/day) are not recommended in the management of diabetes.”
So we can see the ADA is firm and clear in the belief that individuals, even those with type II diabetes, must consume at least 130g of carbohydrate each day; otherwise they are consuming a low-carbohydrate diet.
With me so far?
Now in the study above, the researchers specifically cite the same January 2006 position statement as their reference for their statement “Diets that provide low carbohydrate, low fiber, and high saturated fat contribute to disease complications in diabetes and are not recommended ;” with reference 12 being Standards of Medical Care in Diabetes – 2006. Diabetes Care 2006; 29(suppl 1):S4-42.
I am making a point of this citation because the researchers state their objective in publishing this paper as “…the specific prevalence of low-carbohydrate diet trend in patients with T2DM has not been documented. Thus, the objectives of the present study were to examine baseline dietary, physiologic, and demographic information from adult patients with poorly controlled T2DM in an academic medical center.”
So far, so good.
The researchers recruited 163 potential subjects from eight physicians who agreed to participate and help find subjects, along with the use of intranet messages and flyers to find patients willing to participate if the individual’s physician cleared them to be screened as a candidate. Then these 163 candidates were included or excluded by telephone interviews, HbA1c screening and inclusion/exclusion criteria. The screening resulted in 40 subjects accepted and enrolled in the Diabetic Education Eating Plan Study.
The exclusion criteria included this curious reason to reject a subject, “Currently adhering to a low-carbohydrate diet such as the Atkins Diet or the South Beach Diet.”
The reason given why this would exclude someone from enrollement in the study? From an intervention perspective, this exclusion was because these diets are low in all sources of carbohydrate, and modification of the type of carbohydrate (GI) will have a limited effect on glycemic load (GL) and therefore on HbA1c.
Okay, so those already eating low-carbohydrate diets were excluded because modifying their dietary carbohydrate within the study protocol for GI and GL of carbohydrates won’t result in the data showing a benefit to HbA1c.
In fact, this is a very subtle admission that the dietary intervention the researchers are about to subject their participants to is not better for them if they are already following a low-carbohydrate diet.They excluded subjects already doing a low-carbohydrate diet because carbohydrate restricted diets are already low GI and GL; those individuals are already assumed to be benefiting from lower GI and GL, and increasing their carbohydrate actually risks the trial data in the future!
Basically, from what I can see, the researchers excluded these individuals because there is adequate data available that tells them if they modify the diet to be higher in carbohydrate, even though intake will be within the protocol definition of lower GI and GL, these folks will at risk to be negatively affected; and the potential for such would negatively affect the data outcome seeking to show benefit from dietary intervention in the trial.
So then, how did the researchers – after painstakingly excluding those following a low-carbohydrate diet – conclude their study subjects were eating a low-carbohydrate diet?
In their conclusions they state, straight out “All participants stated that they were engaged in dietary management of their diabetes, although they specifically stated they were not currently following on of the popular low-carbohydrate diets and therefore met study criteria”
They reported average intake was 159g carbohydrate per day, it did not fall below the ADA minimum intake of 130g, nor meet the ADA definition of a low-carbohydrate diet, yet these inconvenient facts do not stop the researchers from concluding this was a low-carbohydrate diet.
“Low-carbohydrate and high-fat intakes were observed at baseline among most participants with poorly controlled T2DM at our primary care clinic, despite the exclusion of patients following low-carbohydrate dietary programs such as the Atkins and South Beach diets.”
If that wasn’t enough, they continued, “Our obervations may be representative of many other patients with T2DM, and perhaps of a trend in the wake of the low-carbohydrate diets. Such a diet likely has cardiovascular implications for patients with T2DM, obesity, hypertension, and hyperlipidemia. Although many researchers are advocating this low-carbohydrate approach to diabetic management, more research is needed to determine the effect of this dietary recommendation on other macronutriets such as saturatred fat and fiber.”
Oh, and it keeps getting better – “We found saturated fat intake to be more than twice that of the American Heart Association recommendation. We speculate that, when reducing carbohydrate intake to control weight and hyperglycemia, participants appeared to have replaced the energy they previously got from carbohydrate with energy from fat. Further, participants did not choose to replace carbohydrates with the monnounsaturated or polyunsaturated fats that have been shown to be cardioprotective. The ADA recommends a diet with less than 7% saturated fat content for people with diabetes. It is well understood that saturated fat is one of the main factors contributing to elevation of low-density lipoprotein cholesterol, which can increase risk of cardiovascular disease and overall inflammation.”
On the one hand we have a population of subjects that specifically stated they’re not following a low-carbohydrate diet and their reported intake of carbohydrate confirms they are eating more than 130g of carbohydrate a day as insisted upon by the ADA; then, on the other we have a team of researchers saying this dietary patten is a low-carbohydrate diet; who then go on to warn of dire consequences, even though their references and citations confirm their subjects are not eating a low-carbohydrate diet.
And this made it through peer-review?
This was accepted and published?
What the baseline data clearly shows is their study population is consuming a crappy diet.
But hey, don’t let inconvenient facts deter a good assumption!
The fact is, one simply does not consume an average glycemic index [GI] of 80.7 (based on referent white bread = 100), and glycemic load [GL] of 133.62, if they’re following a low-carbohydrate diet. No can do.
Add to that, a carbohydrate intake of an average 159g daily exceeds the ADA minimum of 130g per day!
But, the sad fact is, there is a lot of mileage to be gained if you can find a way to include, talk about and then discredit low-carbohydrate or carbohydrate restricted diets as a therapy for type II diabetes.
Just call whatever it is you find “low-carbohydrate,” point out all the negative potential problems you can think of, cite and promote the ADA diet as ideal, and don’t forget to ignore all data from the studies available that resulted in statistically significant findings of benefit – and, guess what? You’ve found the recipe for successful publication these days!
The researchers did not include any acknowledgement of the glaring, fatal flaw in their conclusion that the dietary pattern of their subjects was the cause their elevated HbA1c and concurrent complications. They assumed that it was because of the “low carbohydrate” diet, providing an average 159g of carbohydrate each day.
Why is this a fatal flaw?
The researchers did not investigate their subject populations progression of diabetes since diagnosis. That is, they did not seek to answer the question – are our subjects better or worse today than when they were diagnosed? They didn’t seek to know if their subjects diabetes had progressed or improved since diagnosis – instead they assumed the HbA1c at 8.3%, hyperlipidemia, hypertension and other associated complications observed was a consequence of of the reported dietary patten instead of investigating their previous measures of HbA1c, cholesterol, blood pressure, etc.
They simply do not know if their subjects diabetes is worse or better than it was at diagnosis, or at any point previously in their history, because they didn’t bother to look.
It was just so much easier to assume the observed complications and poor control were such because the of their dietary pattern.
Intellectual honesty demands we insist researchers accurately reflect their findings in their publications; it means we must not accept shoddy work or warnings of impending doom that are based on nothing more than assumptions.
Because the researchers did not review history or previous test results in their population (HbA1c, cholesterol, blood pressure) to determine if the reported dietary pattern is exacerbating the observed diabetic complications, it is nothing more than an assumption that the reported baseline diet is the reason for their complications.
Quite frankly the data included actually suggests that both quality and absolute gram intake of carbohydrate matters. But saying that would mean suggesting the ADA minimum intake of 130g is too simplistic and perhaps even too high. Remember, they excluded those already consuming a low-carb diet because they would not realize a benefit to their HbA1c in the study underway.
We know – this is something not argued within the diabetes community at all – that carbohydrates directly influence blood sugars; they raise blood sugars. As evidenced by the findings at baseline – when consumption of carbohydrates is such that glycemic index and load is frighteningly high, while absolute gram intake is moderate and above current recommendations, unacceptably high HbA1c (indicative of chronic hyperglycemia), hyperlipidemia, hypertension and other complications may be indicative of an overall poor dietary pattern in patients trying to control blood sugars while meeting ADA minimum intake of 130g or more carbohydrate each day.
But the researchers don’t take this approach.
Nor do they acknowledge what they don’t know – was this level of carbohydrate and fat, even with higher than desired GI and GL, resulting in improvement or progression of diabetes since diagnosis?
They don’t know.
We don’t know.
They didn’t ask.
They should have.
Or they should have at least acknowledged it was premature to make the assumption the dietary pattern reported for carbohydrates and saturated fat was the cause of the complications observed at baseline in this population.
The bottom line is that this paper is an intellectual disgrace and impedes the progress of science. Perhaps, as a friend of mine suggested this morning an erratum needs to be included to say…the purpose of this study is to examine whether Nutrition is a properly peer-reviwed publication.