Archive for July, 2006
Sometimes I receive emails that are a bit amusing. Yesterday, I received a number emails asking if I was up to the task of reporting on the results from a study mentioned in Sally Squires’ column, the Lean Plate Club, in the Washington Post.
The article, ‘Good’ Carbs To the Rescue, highlighted findings published in the May 1 issue of the American Journal of Cardiology in the paper, Comparison of Coronary Risk Factors and Quality of Life in Coronary Artery Disease Patients With Versus Without Diabetes Mellitus. One email asked if I truly believed in reporting the findings from studies contrary to my own beliefs about diet and nutrition.
To answer that simply – yes, I can, I do and I have in the past in this column!
With regard to this particular study – I hadn’t seen it previously and can say after reading through the paper, I did find the results intriguing, yet lacking in the detail expected when subjects with diagnoised diabetes are included in a study that specifically modifies diet as part of the design.
In the above study, researchers sought to investigate the effect of dietary modification in those with coronary artery disease (CAD), some of the subjects included also had diabetes. The subjects included 440 individuals – 347 men (55 with diabetes) and 93 women (36 with diabetes). All were placed on a very low-fat vegan/vegetarian diet (target 10% or less calories from fat), provided weekly counseling and support, and advised to exercise and practice stress management daily as they were followed for one-year.
For the purpose of this article, I am going to focus on the subjects with diagnoised diabetes since the article written by Ms. Squires focused on this group in her opening sentences – “People with Type 2 diabetes are advised to limit carbohydrates because of worries that too many carbs could overtax the body’s dwindling insulin production and lessen its ability to process glucose…Now some scientists are asking if a very-low-fat diet rich in healthy carbohydrates — whole grains, beans, fruit and vegetables — might be another option.”
Over the period of one-year, the researchers tracked changes in BMI, weight, cholesterol levels, blood pressure, exercise capacity, changes in medication requirement, and physical and emotional health.
Unfortunately, the researchers did not track, or at least did not publish, changes in fasting glucose, glucose tolerance, insulin levels, HbA1C or other risk markers considered important to evaluate in those with diabetes.
This lack of detail makes the data that is published in the study much more difficult to evaluate for efficacy in those with diabetes.
As I noted, the researchers did publish details about the number of subjects taking diabetic medications at baseline and at one-year. Of the 91 followed for the year, 5 dropped out so we have no data for their medication changes; 62 experienced no change in their medication regiment; 12 discontinued their diabetes medications; 6 no longer required insulin but did require an oral antiglycemic; and 6 experienced a worsening of their condition that required medication not taken at baseline.
Why lacking details are important:
- Of the 62 who did not change medication, 16 started with no medication and remained free of diabetic medication requirements. That’s a good thing and I believe this sub-set should have been reported as a separate group.
- Of the remaining 46 reported as “no changes” in medication, we are provided no detail about dosing requirements! While their medication regiment (oral or insulin) may not have changed, we have no details as to whether their dosage increased, remained the same or decreased during the period of one year. This data is critical to understand if this type of dietary intervention is slowing progression of the disease or not.
- In the 6 subjects who experienced a worsening of their condition we are also not provided details to better understand why their condition may or may not have been made worse by the diet and/or lifestyle interventions of the study.
In her column, Ms. Squires writes, “Blood levels of low-density lipoprotein (LDL), “bad” cholesterol that raises heart disease risk, dropped. Levels of protective high-density lipoprotein (HDL) didn’t drop, and unhealthy fats known as triglycerides didn’t rise, as some researchers had feared.”
However, when we read through the data, the reduction in LDL cholesterol did not reach statistical significance in those with diabetes; HDL remained unchanged in the diabetic women and declined slightly in the diabetic men (not statistically significant); and the triglycerides declined slightly in the diabetic men and rose in the diabetic women (not statistically significant), remaining well above the “high risk” target of 200mg/dl in both the men and women.
The last piece of critical data missing is details about the diet composition. We are provided only one small piece of data – the fat content, as percentage of calories. The fat content was 14.2% in the diabetic men and 19% in the diabetic women when they started the dietary modification (baseline). This was significantly modified in the trial – at one-year the men consumed 6.4% of total calories as fat and the women 8.9% of calories as fat.
What we don’t know is just as important – how many calories did they consume at baseline and after one-year? How much protein? How many carbohydrates? How much fiber? What type of carbohydrates? What did the micronutrient profile look like at baseline and one-year? What did they eat to achieve the consumption pattern? How did calorie intake and composition change from baseline to one-year? There are more unknowns here than I believe is acceptable in a study modifying diet!
My last concern with the study is that it was a multi-faceted intervention: diet, exercise, stress management and intensive support. On its face, these modifications are all considered good interventions and worthy of investigation in a controlled trial. The problem lies with teasing out which ones were meaningful in the results. Was it the diet, the exercise, the reduction of stress, the support, the weight loss from diet and exercise, or a combination of two or more? We don’t know because each potentially plays a role and each is considered a “confounding variable” if not controlled for specifically.
While I applaud the researchers for convincing a good number of individuals to stick with this trial for the year – a very low-fat vegan/vegetarian diet is extremely difficult to follow faithfully – the fact remains the published data remains lacking in sufficient data and control that could have been included.
Noticably absent is critical data for those with diabetes – levels of glucose, insulin and HbA1C; glossed over is the fact that in those with diabetes, LDL was not reduced significantly, HDL remained low in both men and women and men had a minor decrease in the year, and triglycerides remained at levels considered “high risk,” and actually rose in the women with diabetes.
The lack of statistically significant improvements in those with diabetes means we should look at this study with caution because what we have here is study that is not as impressive as we’re led to believe in the media reporting of the findings when we actually go to the data and read through the findings ourselves.
I was a bit surprised by the conclusions reached in the recent issue of the Archives of Internal Medicine – Comparison of 4 Diets of Varying Glycemic Load on Weight Loss and Cardiovascular Risk Reduction in Overweight and Obese Young Adults – in which researchers concluded that “Both high-protein and low-GI regimens increase body fat loss, but cardiovascular risk reduction is optimized by a high-carbohydrate, low-GI diet.”
So, as you may have guessed – I was off to reading the full-text and data to understand how the conclusion was reached.
As suspected, total cholesterol and LDL were the ever “all important” markers used to determine cardiovascular risk reduction.
Each time I come upon another study that fails to include other potent measures of cardiovascular risk as part of the conclusions, I’m less surprised. Some days it seems the diet-heart-lipid hypothesis is so entrenched in the conventional wisdom we’re doomed to just keep on keeping on with it, stumbling along while ignoring other critical markers in our “vein” [pun intended] attempt to convince the population to eat less fat while continuing to eat a diet rich with carbohydrate!
Who are they kidding?
For one thing, the study was just twelve weeks – as we hear so often from the low-carbohydrate diet critics, such a short period is way too little time to make such a sweeping conclusion that reduction of cardiovascular risk is “optimized” by a diet. And you know what, twelve weeks is too little time! I’ve never had an issue with that criticism leveled at studies of short duration for low-carbohydrate diets. I do take issue with dietary studies of similar short duration touted as examples to “optimize” reduction of cardiovascular risk!
Add to that the researchers make no mention of the insignificant reduction to blood glucose, the miniscule increase in HDL, the almost non-existent reduction in triglycerides nor the inconsequential down tick in glucose levels. These other risk markers had no spectacular improvements, yet the researchers concluded the high carbohydrate-low GI diet offered “optimized” cardiovascular risk reduction.
Reducing the risk of cardiovascular disease is a lot more than just getting total cholesterol and LDL heading south – I believe they also need to happen in conjunction with other overall improvements – significant reduction in triglycerides, improved glycemic control, improved insulin and improvements in TC:HDL and HDL:TG. At the end of the day, LDL may not be the end-all be all marker we make it when we look at the bigger picture with what may be more important risk markers.
While the old guard still holds sway and appears to influence researcher conclusions to focus on LDL and total cholesterol, there is compelling evidence (as I’ve pointed out previously) that we must be investigating other markers if we’re going to truly make a difference in the lives of millions with or at risk for cardiovascular disease.
When we look at the total list of risk markers we find the high carbohydrate-low GI diet was not necessarily the “optimal” diet for long-term cardiovascular health. In fact, none of the diets were all that spectacular with overall improvements to stand out. In this particular study, the results at twelve weeks were so mixed they’re really clinically insignificant in my view, especially if the intent of such studies is to increase our knowledge and significantly impact all markers in those at risk.
If we aspire to take a broader view of risk reduction and seek to really improve overall health, a good example is found in the study published last year by Yancy et al. I highlight this study because of the similar duration and calorie intake with focus on low carbohydrate, which is naturally low for glycemic index and glycemic load, but dramatically different macronutrient mix for consumption of carbohydrate, protein and fat. It is probably the best to use here in an attempt for an apples-to-apples comparison.
Yancy et al included just 38.9g average carbohydrate, 93.5g average total fat and 98.5g protein in 1418 calories; McMillian-Price et al (above) included 200g carbohydrate, 36g total fat and 63g protein in 1438 calories. Yancy et al does not detail consumption of saturated fat, but it’s a fair assumption it was significantly higher for dieters in his study given the total fat intake along with the higher protein intake.
If dietary fat is truly detrimental – especially saturated fat – we should see some major increased risks in those following the diet in Yancy, right?
Funny thing – we find significantly greater improvements in those subjects following the diet in Yancy than we do in McMillan. With one glaring exception – LDL cholesterol. Let’s take a look:
Yancy 131.4kg reduced to 122.7kg (-8.7kg)
McMillian-Price 87.1kg reduced to 82.3kg (-4.8kg)
(to be fair, Yancy et al was an additional four weeks in duration)
Yancy 4.61 reduced to 4.54 (-0.70)
McMillian-Price 4.71 reduced to 4.53 (-0.18)
Yancy .92 increased to .99 (+0.07)
McMillian-Price 1.16 increased to 1.21 (+0.05)
Yancy 2.51 increased to 2.77 (+0.26)
McMillian-Price 2.9 reduced to 2.73 (-0.17)
Yancy 2.69 reduced to 1.57 (-1.12)
McMillian-Price 1.39 reduced to 1.34 (-0.05)
Yancy 5 reduced to 4.5 (-0.50)
McMillian-Price 4.16 reduced to 3.95 (-0.21)
Yancy 2.92 reduced to 1.58 (-1.34)
McMillian-Price 1.19 reduced to 1.10 (-0.09)
Yancy 9.8 reduced to 7.57 (-2.23)
McMillian-Price 4.95 reduced to 4.88 (-0.06)
The question begs – why are we still bent on LDL cholesterol as an end-all-be-all marker of improvement or reduction of risk? It’s clear from the data above that subjects experienced greater overall improvements following the low-carbohydrate diet than they did following the high carbohydrate-low GI diet that was also low in fat and protein.
It’s pretty easy to do the math – McMillian et al provided 22% of calories a fat (36g in 1417 calories) and Yancy et al provided 59.3% of calories as fat (93.5g in 1418 calories).
The subjects in Yancy et al consumed not only relatively more fat (percentage of calories), but absolutely more fat (grams consumed daily) – they ate 3-times the fat as those in McMillian et al. In fact, those in the Yancy et al study consumed more fat than the average American does each day if the American Heart Association numbers are correct at 81.4g total fat per day per person!
They ate more fat and still had greater improvements in the broader list of risk markers, except their LDL increased slightly.
But, after decades of being told it’s the dietary fat we must reduce (with no convincing data), we’re now seeing a transition in the message to eat a diet that is low in fat and low GI, but still rich with carbohydrate. Aside from both diets offering the ability to lose weight, the data above clearly shows that after twelve weeks, other than LDL cholesterol levels, no other significant improvements were found in subjects following the high-carbohydrate/low-GI/low-fat diet.
While it is politically correct to reach such a conclusion, it’s again a great example of how dogma can over-ride hard data. Shouldn’t a conclusion of “optimized” reduction of cardiovascular risk also include HDL? Triglycerides? Glucose? Insulin? TC:HDL ratio? TG:HDL ratio?
The hard data here is that none of the four dietary interventions McMillian et al investigated did much of anything in twelve weeks other than allow for some weight loss and two of the four resulted in a reduction in LDL.
Simply put – that’s not enough time nor improvement to make a sweeping and strong conclusion that a high carbohydrate, low-GI diet (the one that reduced LDL the most) optimizes cardiovascular risk reduction!
The American Heart Association has yet to provide a single day (or seven-day) menu to provide details to the public or healthcare providers about how to follow their new 2006 Diet & Lifestyle Recommendations issued last month.
In my June 22nd challenge, I placed a $1,000 reward for anyone who can design a menu that meets the AHA guideline restricting saturated fat to less than 7% of total calories while also meeting all essential nutrient requirements (vitamins, minerals, trace elements, essential fatty acids and essential amino acids) and is within the AHA guidelines for cholesterol, sodium and types of foods to include (or avoid).
I almost expected the AHA would immediately submit a menu to my challenge to prove it can be done. I mean, hey, they have a team of nutrition experts to call on and compile such a menu fairly quickly (if it can be done), right?
Well, instead of posting a menu to help someone understand how to follow their new guideline, they’ve included a guideline detailing how many servings of each food group should be included in a daily menu to comply with their guidelines. For those taking part in the challenge, it is a requirement to follow all AHA recommendations, including this new set of information regarding number of servings from each food group.
Which places those who have already submitted a menu that failed at a disadvantage – the AHA hadn’t provided clear guidance previously at the start of the challenge to guide the design of a menu. So, in the spirit of good sportsmanship, I am extending an invitation for re-submission of a revised menu to those who previously submitted a menu who would like to try again with a menu based on this more detailed information.
Since the challenge menu requires 1956-calories (+/- 5 calories), designed for a female-30, the following guideline is provided by the AHA:
6-8 servings a day; half from whole grain sources
4-5 servings a day
4-5 servings a day
- Fat-free or low-fat dairy:
2-3 servings a day
- Lean meats, poultry, seafood:
Less than 6-ounces (cooked) a day
- Fats and oils:
2-3 servings a day
- Nuts, seeds and legumes:
4-5 servings per week
- Sweets and added sugars:
Less than 5 per week
Details about what constitutes a serving size is available on the AHA website.
To date none of the menus I’ve received comply with the above serving recommendaitons issued by the AHA. And, so far none I’ve finished analyzing meet the challenge requirement to be within the AHA guidelines and provide for essential nutrients. If you’ve previously submitted a menu and it was found to be deficient, you may try again at this time since the AHA has provided more detail since the challenge started. If a menu submitted is currently under review, and is not within the above guideline, I will return it to you for revision to allow you to create a menu within the above standard issued by the AHA.
Oh, and if you haven’t yet tried to do a menu – go for it, I have $1,000 sitting here for the first person who creates a menu that includes the above servings for each food group and meets all the other challenge requirements detailed previously!
This week’s Archives of Internal Medicine had an interesting study published – An Assessment of Incremental Coronary Risk Prediction Using C-Reactive Protein and Other Novel Risk Markers: The Atherosclerosis Risk in Communities Study – in which researchers investigated the clinical utility of 19 “novel” risk markers for predicting cardiovascular disease compared with the traditional risk markers currently used by clinicans in practice today.
The cover graphic quickly provides a glimpse at the traditional risk markers and the “novel” markers currently making headlines as potentially important as part of the risk assessment with patients.
After reviewing these novel markers compared to the traditional risk markers, the researchers concluded that “Our findings suggest that routine measurement of these novel markers is not warranted for risk assessment. On the other hand, our findings reinforce the utility of major, modifiable risk factor assessment to identify individuals at risk for CHD for preventive action.”
In an accompanying editorial, Predicting Cardiovascular Risk, Dr. Donald Llyod-Jones included a stunning comment followed by a critical question, “It is possible that, to date, we have examined the wrong novel risk markers. Should we seek as yet undiscovered markers that will improve risk prediction substantially when added to established risk factors?”
He continued with a caveat – “Such markers will need to be highly associated with CHD, uncorrelated with established risk factors, have a reasonable prevalence of risk-producing levels in the population, and not increase competing risks for other diseases. Where will we find such markers?”
But then, adds more questions, “Should we start again and create new CVD risk prediction models without guaranteeing inclusion of established risk factors? Would this be of clinical value? How would we know what to treat?”
And then asks an incredibly important question, “Do we perhaps need a different goal? Rather than identifying high-risk individuals for drug therapy, should we try to optimize identification of low-risk individuals and attempt to move the population profile toward this ideal through public health interventions?”
As I read through Dr. Llyod-Jones’ editorial I was struck by the questions and the simplicity of exploring alternative risk prediction models. The literature is rich with data – much largely ignored when it comes to heart disease since we’re entrenched in the belief that cholesterol and saturated fat are the culprits in heart disease.
But if we start with his last item – identifying low-risk individuals – we find something potentially ground-breaking, that’s often not considered as we debate how to assess risk for heart disease – who can provide us with a good picture of long term health?
Centenarians – those who live to be 100 or older around the world. You don’t live to be 100 without something important going on – and I contend, it’s not just genetics.
We know those who live to be 100 or more are a very diverse group – their longevity isn’t consistently based on moderate alcohol consumption, smoking habits, country of origin, or ethnicity. And we also know that cholesterol values, overall diet and levels of activity vary greatly. In fact, we know there are only three things that link centenarians around the world – relatively low blood glucose, strong insulin sensitivity and low triglycerides.
That’s it – in study after study, these three things are the only three things that are shared “common denominators” in those 100 or older.
The question then begs – if strong insulin sensitivity, low triglycerides and low blood glucose are the common ties-that-bind centenarians together as a group, should these metabolic markers be our new starting point to understand and reduce the risk of heart disease?
A quick review of the literature suggests the answer is “yes.”
An article in the May 16, 2006 issue of New Scientist had an interesting quote from Dr. Andrzej Bartke, a researcher at Southern Illinois University, “Insulin resistance is a risk factor for just about any problem you don’t want to get: diabetes, atherosclerosis, cancer. It’s sort of intuitive that the opposite situation would be beneficial.”
The opposite, of course, is strong insulin sensitivity.
But we do have to ask – does strong insulin sensitivity confer any health benefit? In reverse, is there evidence that higher levels of insulin, and thus blood glucose and triglycerides, increase heath risks? Basically, does higher insulin, blood gluocse and triglycerides have a detrimental effect?
Interestingly, several studies show the atherogenic effects of high blood glucose and insulin:
2002 – American Journal of Hypertention; Correlates of aortic stiffness in elderly individuals: a subgroup of the Cardiovascular Health Study
“Mean aortic pulse wave velocity (850 cm/sec, range 365 to 1863) did not differ by ethnicity or sex. Increased aortic stiffness was positively associated with higher systolic blood pressure (SBP), age, fasting and 2-h postload glucose, fasting and 2-h insulin, triglycerides, waist circumference, body mass index, truncal fat, decreased physical activity, heart rate, and common carotid artery wall thickness (P < .05)…In these elderly participants, aortic stiffness was positively associated with risk factors associated with the insulin resistance syndrome, increased common carotid intima-media thickness, heart rate, and decreased physical activity measured several years earlier.”
March 2001 – American Journal of Epidemiology; Metabolic syndrome and ischemic heart disease in elderly men and women
“In both men and women, three uncorrelated principal components were identified, representing a central metabolic factor (body mass index, fasting and 2-hour serum insulin, high serum triglycerides, and low HDL cholesterol), a glucose factor, and a blood pressure factor. In a multivariate model with age and sex, all three factors were significantly associated with IHD by electrocardiogram criteria; central metabolic factor, glucose factor, blood pressure factor, age (10 years), and female sex. Similar results were obtained in analyses using clinically manifest IHD as the outcome. These results support the thesis that the metabolic syndrome exerts effects through different risk factors by different mechanisms.”
April 2000 – European Journal of Clinical Investigation; Effects of glucose ingestion on cardiac autonomic nervous system in healthy centenarians: differences with aged subjects
“In aged subject (AS), but not in healthy centenarians (HC), the baseline low frequency/high frequency ratio (LF/HF) correlated significantly with BMI, waist-hip-ratio (WHR), fasting plasma insulin, and norepinephrine concentration. Glucose ingestion was associated with a significant rise in LF/HF ratio in both groups studied but per cent changes in glucose mediated stimulation of LF/HF was lower in HC than in AS…Our study demonstrates that basal- and glucose-stimulated LF/HF, an indirect index of cardiac sympatho-vagal balance, are lower in HC than in AS.”
January 2000 – European Journal of Clinical Investigation; Insulin resistance, lipid and fatty acid concentrations in 867 healthy Europeans. European Group for the Study of Insulin Resistance (EGIR)
“The associations of fasting triglycerides with the M-value and with nonesterified fatty acid (NEFA) at steady state were independent of each other. All these associations were independent of obesity and geographical location…The results in this large cohort of healthy European subjects suggest that triglyceride concentrations depend upon both insulin’s gluco-regulation (estimated by glucose uptake) and antilipolytic insulin action (measured by NEFA levels) during an euglycaemic clamp.”
April 1998 – Annals of Internal Medicine; Metabolic risk factors worsen continuously across the spectrum of nondiabetic glucose tolerance. The Framingham Offspring Study
“Multivariable-adjusted mean measures of risk factors and odds ratios for obesity, elevated waist-to-hip ratio, hypertension, low levels of high-density lipoprotein cholesterol, elevated triglyceride levels, and hyperinsulinemia showed continuous increases across the spectrum of nondiabetic glucose tolerance. Although a threshold effect near the upper range of nondiabetic glucose tolerance could not be ruled out for triglyceride levels in men and for insulin levels 2 hours after oral challenge in men and women, no other metabolic risk factors showed clear evidence of thresholds for increased risk…Metabolic risk factors for type 2 diabetes mellitus and for cardiovascular disease worsen continuously across the spectrum of glucose tolerance categories, beginning in the lowest quintiles of normal fasting glucose level.”
“Results of the present study suggest that both hyperinsulinemia and “hypoinsulinemia” are independent indicators of CHD. Furthermore, it is proposed that the relationship between CHD and fasting insulin is U-shaped, whereas that between CHD and postglucose insulin may be J-shaped.”
“No index of overall obesity, fat patterning, glucose/insulin metabolism, and/or SI, was independently related to the plasma concentration of HDL-C after controlling for any one of the other two. Direct measurement of glucose/insulin metabolism and insulin sensitivity (SI), as well as fat patterning, provides information on their relative associations with CVD risk factors. The measures of glucose/insulin metabolism and SI were more consistently related to dyslipidemia and hypertension than were the overall obesity and fat patterning in this healthy population.”
March 2006 – Journal of the American Geriatric Society; Impaired fasting glucose is associated with increased arterial stiffness in elderly people without diabetes mellitus: the Rotterdam Study
“In the total cohort, fasting glucose was strongly associated with carotid distensibility…IFG is related to arterial stiffness in elderly subjects. An advanced stage of arterial stiffness, comparable with that of subjects with DM, is only reached at the age of 75.”
April 1994 – Arteriosclerosis and thrombosis; Hyperinsulinemia predicts multiple atherogenic changes in lipoproteins in elderly subjects
“Baseline insulin level was not significantly associated with the development of high LDL cholesterol or low HDL cholesterol levels. Baseline insulin was associated with the development of hypertriglyceridemia.”
January 1991 – Arteriosclerosis and thrombosis; High fasting plasma insulin is an indicator of coronary heart disease in non-insulin-dependent diabetic patients and nondiabetic subjects
“The results suggest that hyperinsulinemia is an indicator of CHD in both NIDDM patients and nondiabetic subjects. Hyperinsulinemia may be directly atherogenic, but it is more probable that hyperinsulinemia reflects insulin resistance, which may be a factor enhancing atherogenesis by causing adverse changes in many CHD risk factors.”
November 2002 – International Journal of Cardiology; Fasting insulin levels independently associated with coronary heart disease in non-diabetic Turkish men and women
“Hyperinsulinemia (i) may provide information on the coronary heart disease likelihood over and above that provided by the other risk factors, including HDL-cholesterol, and (ii) may contribute, within the frame of insulin resistance, to the coronary heart disease risk independently of the classical risk factors.”
January 2006 – Diabetes Care; Relation Between Blood Glucose and Coronary Mortality Over 33 Years in the Whitehall Study
“A threshold model with linear slope best described the dose-response relationship between postload blood glucose and CHD mortality risk.”
The above are just a dozen studies randomly selected that are available in the literature – many more exist and are easily accessible in PubMed.com. To me, they highlight the pressing need to step back from our obession with dietary fats, which are, on their own, pretty much metabolically neutral, and re-evaluate the influcence our diet rich with carbohydrates, especially refined carbohydrates, is exerting on our long-term health.
This isn’t rocket science – a very basic understanding of metabolism and metabolic pathways explains exactly how and why excessive carbohydrate consumption contributes to not only obesity, but insulin resistance, and thus heart disease.
Some of the most depressing studies available today are those investigating the cardiovascular health of children, already well on the road to diabetes, cardiovascular disease and a reduced life expectancy.
June 2003 – Obesity Research; Fasting plasma insulin modulates lipid levels and particle sizes in 2- to 3-year-old children
“Fasting insulin level was positively correlated with triglyceride levels and inversely correlated with HDL-cholesterol level in boys. Higher fasting insulin level was also correlated with smaller mean HDL particle size in both boys and girls and smaller mean LDL particle size in boys. The associations of fasting insulin level with triglyceride and HDL-cholesterol levels and HDL and LDL particle size remained significant after multivariate regression adjustment for age, sex, and BMI or ponderal index. Fasting insulin level is associated with relative dyslipidemia in healthy 2- and 3-year-old Hispanic children.”
Two and three year old children, already experiencing the health damaging effects of high insulin and high triglycerides!
Yet, the “traditional” risk factors [see graphic above] do not include insulin levels, blood glucose or triglycerides in weighing an individuals risk for heart disease. It is only when an individual has progressed to diabetes that their metabolic condition is acknowledged to be the risk factor it is. The above studies clearly demonstrate the detrimental effects long before someone presents with diabetes!
While the study above explored the value of 19 additional potentially useful risk factors, noticiably absent are three that should have been considered – insulin, glucose and triglycerides.
I’d like to applaud Dr. Llyod-Jones for pointing out that our current thinking may be impeding our efforts to reduce the risk of cardiovascular disease.
Staring us in the face is the potent value of measuring insulin and insulin sensitivity, blood glucose and triglycerides – these, at low values, are the shared traits in centenarians around the world; and it is these same markers, at elevated levels, that are found again and again in studies where cardiovascular disease is an issue.
We’ve spent decades – and billions of dollars – convincing ourselves it is dietary fat that increases the risk of heart disease. I really have to wonder how much time we’re going to continue to demonize dietary fat and cholesterol, while ignoring the data that insulin, blood glucose and triglycerides are strong predictors of cardiovascular disease and/or longevity.
How much longer can we afford to ignore the increased consumption of carbohydrates in the US? How much longer can we afford to ignore the lasting damage high insulin, blood sugar and triglycerides exact on our children and their long-term health?
How much longer until Americans wake up and demand the leading health organizations take the evidence seriously enough to step back and question the current paradigm, evaluate the role of excessive carbohydrate in disease, and base recommendations on science not dogma?
MSNBC reported on a study published in the July issue of Diabetes Care – A prospective study of dairy intake and the risk of type 2 diabetes in women conducted by researchers at UCLA.
The article, Low-fat dairy may lower women’s diabetes risk, opens with “A diet that includes lots of low-fat dairy products may lower the risk of type 2 diabetes in women, new research suggests,” and continues with details of the just published study where researchers “looked for the relationship between type 2 diabetes and dietary levels of dairy foods and calcium in 37,183 women in the Women’s Health Study. A total of 1,603 women developed diabetes during an average follow-up of 10 years.”
The lead researcher, Dr. Simin Liu, from the University of California Los Angeles School of Public Health noted he and his colleagues undertook the investigation because a series of recent studies suggests that a high level of dairy foods in the diet may lower the risk of being overweight or developing insulin resistance syndrome, studies that have examined the link between these factors and diabetes risk are sparse.
When I first started to read through the data, I was struck by just how many confounding factors they “adjusted” to reach their significant findings!
- smoking status
- physical activity
- family history of diabetes
- alcohol consumption
- history of hypertension
- use of hormones
- high cholesterol
After “adjusting” for these inconvenient variables, the researchers concluded “A dietary pattern that incorporates higher low-fat dairy products may lower the risk of type 2 diabetes in middle-aged or older women.”
They didn’t add IF you’re normal weight, don’t smoke, are active, don’t have a family history of diabetes, drink in moderation, don’t have a family history of high blood pressure, aren’t using hormones and don’t have high cholesterol. Basically, they forgot to add the findings apply to those who are in good health!
Which begs the question – was it the inclusion of dairy or was it an overall better dietary and lifestyle pattern that kept these women in good health?
The problem with studies such as this is they’re focused only on one particular in a dietary pattern that includes a wide variety of other foods. Add to that lifestyle, genetics and family history and it’s impossible to say with any certainty that one particular food or food group is protective against disease. It’s a leap of faith to say eating more dairy lowers the risk of type 2 diabetes without considering those confounding variables that were conveniently “adjusted” out of the equation.
I hate to say it, but this isn’t science. If you ask me, it seems more like a manipulation of data to promote the dairy industry and the consumption of milk and dairy products.
Hey, I like dairy – I eat natural cheese, whole milk yogurt and occassionally even enjoy some good homemade ice cream – but do I need to include dairy to prevent diabetes? No
Reducing the risk of diabetes comes down to two things – eating a nutrient-rich diet and staying active. Sure, dairy can be part of that equation, but it’s not an essential food, holds no magical metabolic protection and is an absolute nightmare for those who are lactose intolerant.
In the Lancet this week, researchers published a chilling finding – Diabetes confers an equivalent risk to ageing 15 years – in Relation between age and cardiovascular disease in men and women with diabetes compared with non-diabetic people: a population-based retrospective cohort study.
As reported in Forbes, “…the most striking numbers in the report involved life expectancy. People with type 2 diabetes who were also classified as being at moderate or high risk for cardiovascular disease died an average of about 18 years earlier than non-diabetics, the researchers found.”
I don’t know about you, but I find it disturbing that we now estimate one-third of adults in the United States have or at risk for type II diabetes and we’re still making the same recommendations for diet that have done nothing to reverse, or even slow the ever-increasing incidence of the disease in the last thirty years.
Throughout the medical and scientific literature there is a wealth of data correlating glycemic control, and insulin and blood glucose levels, with cardiovascular disease. These findings are consistent in those with and without type II diabetes.
Back in 1988, the Paris Prospective Study, published in the International Journal of Obesity, found “The strength of the association of blood pressure to the risk was reduced when BMI increased. By contrast, the association of blood pressure to the risk remained linear when plasma insulin level rather than BMI was considered. Plasma insulin level was a more sensitive marker of CHD risk than glucose intolerance in the overweight group. Moreover, in this group, the relation to CHD mortality risk was stronger for plasma insulin level than for blood pressure.”
In 1998, the Journal of Clinical Endocrinology & Metabolism published a study in which researchers concluded that “In conclusion, approximately one of every five healthy, nonobese subjects in the most insulin-resistant tertile, followed for approximately 5 yr, had a serious clinical event. These data highlight the importance of insulin resistance as a predictor of CVD.”
In JAMA in April 2004, researchers published findings from subjects with normal glucose tolerance – a cohort of 234 men were investigated and the researchers concluded that “For patients with NGT and different extents of atherosclerotic disease, postload glycemia and HbA1c level are not equally distributed but are significantly higher in those with more severe disease. This suggests that the glycemic milieu correlates with the cardiovascular risk according to a linear model.”
Let’s not forget, earlier this year, a study was published after following 18,403 men for thirty-three years. The researchers found that ten years into the study, heart disease mortality started to increase at blood sugar levels above 95 mg/dl, but that those subjects with blood sugar levels below 95 mg/dl showed no increased risk for death from heart disease. After 33-years, the increased risk for heart disease started at blood glucose levels of 83mg/dL – with a linear increase in risk between 83mg/dL and 95mg/dL.
To date, not one study has been published with similar correlations to cholesterol levels.
In fact, the researchers in the above study measured cholesterol levels and found no significant difference in cholesterol levels between those subjects with normal blood sugar, those who were glucose intolerant, and those diagnoised with diabetes. Over thirty-three years it wasn’t the cholesterol levels that mattered – it was blood sugars!
And here we are today, still preaching cholesterol, cholesterol, cholesterol; saturated fat, saturated fat, saturated fat as the only dietary means to reduce heart disease. Folks – it’s not the cholesterol, and it’s not the saturated fat – it’s the blood sugars and resulting insulin resistance from years of excessive carbohydrate consumption!
Every single time you consume more carbohydrate than your body needs, it’s excessive – and it’s placing a burden on your metabolism to deal with the excess.
Just how long do you think your metabolism can keep humming along with too much blood sugar? How much time passes before repeated highs in blood sugars, and resulting highs in insulin, do damage to your cardiovascular system?
Don’t fool yourself into thinking there are “good carbs” and “bad carbs” – there are only carbohydrates; some providing essential nutrients with a small amount of carbohydrate and others that are nutritionally bankrupt and/or providing too much carbohydrate-load to the body at one time. Both simple and complex carbohydrate is metabolized to glucose in the body – the former just faster than the latter.
Eating too many complex carbohydrates results in the same level of blood glucose as eating too many refined or simple carbohydrates – and both result in a higher demand for insulin to stablize blood sugars. Even the American Diabetes Association (ADA) acknowledges “[t]he total amount of carbohydrate consumed is a strong predictor of glycemic response.”
Over time, this rollercoaster of high blood sugars, demand for more insulin to reduce blood sugars within a tight range of normal and increasing insulin resistance is damaging to not only the metabolism, but to cardiovascular health. At some point, the body simply has to make compromises when it is assaulted day in and day out by foods that damage its ability to function properly.
The food you choose to eat has a direct and lasting effect on how well your body functions – eat the wrong foods repeatedly and your body and metabolism will be damaged over time. Consume foods that optimize your metabolic function while nourishing your body, and your body will thank you with good health.
Good health is the default human condition – when you find yourself in an unhealthy state, it’s time to assess where you can make improvements to enhance your well-being to restore good health. Our bodies are designed for good health – it’s the normal state we are supposed to enjoy each day! Yet, too many of us accept poor health as normal and convince ourselves that it’s just part of life.
You do not have to accept poor health as your fate.
There are simple modifications one can make to their diet to increase essential nutrient intake and reduce the damaging effects of high blood sugars and insulin. Creating a health enhancing diet starts with eliminating the excessive carbohydrate from your diet – this type of diet is built on our knowledge of the athrogenic effects of high blood sugars and insulin in the body.
In May of this year researchers published the study, The atherogenic potential of dietary carbohydrate, and concluded “High-carbohydrate diets, particularly in the form of high-glycemic index carbohydrate, have the ability to directly induce atherosclerosis. Based on anthropologic facts, the reason for these dietary-induced, insulin-mediated, atherogenic metabolic perturbations are suggested to be an insufficient adaptation to starch and sugars during human evolution. Restriction of insulinogenic food (starch and sugars) may help to prevent the development of atherosclerosis, one of the most common and costliest human diseases.”
The first step is to lay the foundation of nutrients we know are critical for good health – amino acids, fatty acids and vitamins, minerals and trace elements. These essential nutrients are provided by meats, poultry, fish, game, eggs, nuts, seeds, fats/oils, fruits, legumes and non-starchy vegetables.
That’s it – we don’t need any grains for health, and certainly don’t need any refined or processed foods.
But, we like them.
They taste good.
And, we’ve built our entire dietary recommendations around them – established grains as the foundation of our diet rather than nutrient-dense foods. Today, we’re paying the price for our dietary myths – we’re eating excessive carbohydrate and thus, consuming too many calories and getting too fat because of the metabolic rollercoster caused by what we eat. In the process, we’re watching our children suffer with type II diabetes, increasing our dependance on pharmaceutical solutions to our ills and accepting poor health as somehow normal when we age.
With so many “experts” claiming that low-carb and/or controlled-carb diets are unhealthy, it’s difficult to consider their health redeeming benefits. But, a number researchers have published data that supports such a dietary approach as a way to reduce weight, stabilize blood sugars, reduce insulin resistance, reduce HbA1C levels, improve blood pressure and even improve cholesterol. These studies are consistently ignored and dismissed while the established low-fat dogma persists and our health continues to decline.
The only word that describes our current situation in the United States is “crisis” – we are in a national health crisis today and rather than base recommendations on clear data, we’re seeing the leading health authorities dig in their heels and repeat the dietary advice I believe is directly contributing to our declining health.
It isn’t all that difficult to understand that when you tell a population to reduce total fat and strictly limit saturated fat and cholesterol they’re going to eat more carbohydrate to compensate for the calories lost by limiting protein and fat.
Take that to the next step, and it’s not that difficult to understand that shifting consumption of calories to more carbohydrate stimulates more insulin to control higher blood sugars that result from consumption of more carbohydrate. The unintended consequence being that hunger is triggered more often with highs and lows in blood sugar and insulin triggering hunger more often, leading to an increase in calories eaten each day, leading to consumption of more carbohydrates – exacerbating a vicious cycle in the metabolism: the more carbohydrate consumed, the more hunger is triggered, the more calories consumed, the higher blood sugars, the more insulin demanded, the more cells ignore the insulin, the fatter one gets as excess glucose must be shuttled from the blood and is deposited in body fat, the sicker one gets.
The only way to stop that cycle is to stop feeding it – reduce demand for insulin by reducing blood sugars created by excessive carbohydrate intake. An amazing thing happens when one reduces their intake of carbohydrate – they typically reduce calorie intake without specifically trying to create a calorie deficit or count calories; their blood sugars stabilize, their insulin levels stabilize, their cholesterol levels improve; their blood pressure normalizes and they lose weight.
The leading medical organizations and government agencies call this an unbalanced diet and an unhealthy way to eat.
What do you call it?