Insulin resistance cause of cardio-vascular disease

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The following paper, based on literature review (not an independent study!) explains the mechanisms behind cardiovascular diseases: cardiomyopathy, endothelial dysfunction, atherosclerotic plaque formation and coronary heart disease. The main cause = insulin resistance!

"Association between insulin resistance and the development of cardiovascular disease", by
Valeska Ormazabal, Soumyalekshmi Nair, Omar Elfeky, Claudio Aguayo, Carlos Salomon and Felipe A. Zuñiga
Cardiovascular Diabetology201817:122


Quotes:

...epidemiological and pathophysiological studies suggest that hyperglycemia may be largely responsible for CVD. Blood glucose has been reported as an independent predictor of atherosclerosis and blood glucose level greater than 90 mg/dl can lead to atherosclerosis in the carotid artery [125]. Long-term follow up data from patients with type 1 and type 2 diabetes suggest that hyperglycemia is a risk factor for diabetes related diseases and CVDMoreover, it has been suggested by Salvin et al. [126] that a 1 unit increase in the total glycosylated hemoglobin or HbA1C, can increase the risk of CVD by up to 18%. Even in the absence of overt diabetes, impairment in the glucose homeostasis can affect the cardiac autonomic function leading to high risk of cardiac diseases [127].

...
In this sense, recently it has been shown that cyclic ketone bodies preserve “young cardiac phenotype” in old mice [167]. On the other hand, it has been reported that isocaloric ketogenic diet (very low in carbohydrates and high in fats and/or proteins) increases lifespan [168].


Overall, insulin resistance contributes to generate CVD via two independent pathways: (1) atheroma plaque formation and (2) ventricular hypertrophy and diastolic abnormality.

Denise Minger's different kinds of magic

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I love her presentation!

Probably not true!

Who is a bastard who wrote "why"?

Magic rocks!   :)

I highly recommend to listen to her video. She is reviewing some old studies showing therapeutic effects of the very low fat high carbohydrate diets (VLFHC). Low fat means well below 10% preferably about 2%. When I begun my high fat low carb experiment back in 1999, which grew into my ongoing lifestyle nutrition to this day, I was aware that the very low fat natural food diet has been successfully used in halting progression of coronary heart disease and MS. I was familiar about Pritikin and Dr. Swank work. Prior to 1999 I was experimenting with vegetarian nutrition but I found it unpalatable, unless a sufficient amount of fat was added. More than 10%. So for me finding dr. Kwasniewski's Optimal Diet was a "gift from God", or I should say a gift from a friend of mine (Andrew S.)! Kwasniewski's Optimal Diet is high animal fat low carb diet (HFLC). After noticing back then that the VLFHC diets have some therapeutic property, I had many questions (i.e. "question everything"). One of them is about the long term viability and the side effects. Like with every therapy, there may be side effects. Are there side effects of VLFHC diets? How do people do on such nutrition scheme fare in the long term? Longevity issue? Longevity with a robust health or not so well? The same question can also be asked about any other diet, including the HFLC diet.

Unlike most other low carb promoters at that time (1970-ties - 1990-ties), dr. Kwasniewski did acknowledge that a high carbohydrate diet may also be healthy, quoting Japanese rice based diet as an example. He also insisted that, on such a diet (1) fat intake must be limited to abut 10% and (2) a sufficient amount of (lean) protein must be consumed. Insulin sensitivity is very high on such a diet because the intake of fat is very low but the pancreatic insulin secretion is medium. Insulin cannot be too low, due to carbohydrate-based metabolism. Typically it amounts to about 20-30 iu per day, based on my understanding and from reports by t1 diabetics (quoting from memory so verify this before you requote me!)

Dr. Kwasniewski also noticed, based on his patients record, that a particular proportion of macronutrients, consisting of about 35-45% of fat (by calories) and about 45-35% of carbohydrates is particulary unhealthy and makes people prone to developing diabetes and atherosclerotic heart disease. Kwasniewski also noticed that it causes a peculiar form of neuro-degeneration for people in their 40-ties and 50-ties manifesting itself in form character disorder (psychopathy). He called that dietary zone "dangerous middle zone". Pancreatic insulin secretion has to be very high (typically 40-60 iu/day or more) on such a diet in order to overcome the insulin insensitivity induced by the high fat intake.

He also noticed that as soon as you up the total fat intake to above 50% of calories then these pathological effects gradually subside and the diet becomes healthy again, even therapeutically healthy. The widely popular diet he publicized in the 1980-ties, arrived at the macronutrient proportions P:F:C (Protein to Fat to Carbohydrates) in gram per day per 1kg of ideal body weight of 1:3-3.5:0.8 to 1:2-2.5:0.5 . This typically works out at way over 60% (typ about 85%) of fat by calories. Notice that fat has 9kcal/g, glucose 4.5kcal/g and protein 3.5kcal/g (or less if used anabolically). Interestingly, Kwasniewski also found that his patients with coronary heart disease begun reversing and recovering. So his patients with many autoimmune disease such as asthma, rheumatoid arthritis, MS, IBS, and other - also recovered on his diet! Even though the HFLC diet is the exact opposite of the VLFHC diet, it nevertheless produced surprisingly similar (if not greater) therapeutic effects! Notice that the insulin sensitivity (and the effect of fat upon it) becomes irrelevant due to very low intake of carbohydrates. Kwasniewski quoted insulin requirement at this point, to be about 6-10 iu/day. How did he measured it? By observing his type 1 diabetic patients!

What Denise Minger has done, is rediscovering and publicizing that fact that there are 2 dietary zones that have therapeutic properties, not just one diet!

What I would disagree with, is her presumption that the VLFHC diet would:

- "results in healthier gut microbiome long term"

There is not proof or comparison studies done for VLFHC vs HFLC on that, while there is enough reports indicating the long term gut flora deterioration among vegans (I would put refs to Dr. Stanley Bass and Dr. Gian-Cursio reports on Natural Hygienists).

- "may do best for ApoE4 carriers"

No proof either, other than high serum cholesterol which does not always translate to a health risk, except for people eating in the dangerous middle zone.

- "may be able to restore and heal glucose tolerance which does not happen on the high fat..."

This is not true based on my personal observation. Initially yes, HFLC diet did not restore my glucose tolerance, it only allowed my body to bypass the issue by not showering my body with the excess carbohydrates. Whenever I tried to eat a little bit more than 50g of carbohydrates in a day, I would inevitably come to regret it! Carb-headache and nausea. Beer was especially bad for me. However, after about 2 years I noticed that I was able to increase that limit and add more than previously and after about 6-7 years I noticed that my carbohydrates tolerance has been totally restored! For example I can now consume a high carb dinner if I have no other choice without any adverse side effects. I don't do it often, but it is nice to know that my metabolism has completely been restored. I suspect it has to do with the mitochondrial regeneration. It takes about 7 years to regrow and renew most of our muscular tissues from our stem cells. I also found it that initially I had to watch not only the total carbohydrates intake, but I also had to limit the overall caloric intake from fat as well. Initially the total limit was about 1800kcal. Believe it or not that is actually perfectly sufficient for an adult leading an active life on the high fat diet, without any problems (I was 43 in 1999 when I begun HFLC and I weigh 64k, 173cm height) It was as if my metabolic channels were impaired for both macronutrients, for carbs as well as for fat, except the metabolism of fat, being more effective, allowed me to live better and have more energy in spite of the limitations. Again, that restriction is no longer applicable and lifted itself after about 7 years.

Stan (Heretic) Bleszynski

It's sugar not calories!

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New study just published in the Obesity Journal by Dr. Robert Lustig and others.
The results are described in this article:
The science is in: the case for a sugar tax is overwhelming,

Wiki: Soft drink

Quotes:

Is sugar dangerous because it’s calories? Or because it’s sugar?

...we took the added sugar away from 43 obese children who were already sick, to see if they got well. But if they lost weight, critics would argue that the drop in calories or the loss in weight was the reason for their improvement. Therefore, the study was “isocaloric”; that is, we gave back the same number of calories in starch as we took away in sugar, to make sure they maintained their weight.
For nine days we catered their meals to provide the same fat, protein, and total carbohydrate content as their home diet; but within the carbohydrate fraction we took the added sugar out and substituted starch. We took the pastries out, we put the bagels in; we took the yoghurt out, we put the baked potato chips in; we took chicken teriyaki out, we put turkey hot dogs in. We gave them processed food – kid food – but “no added sugar” food. We reduced their sugar consumption from 28% to 10% of their calories. They weighed themselves every day; if they were losing weight, we told them to eat more.
We were astonished at the results. Diastolic blood pressure decreased by five points. Blood fat levels dropped precipitously. Fasting glucose decreased by five points, glucose tolerance improved markedly, insulin levels fell by 50%. In other words we reversed their metabolic disease in just 10 days, even while eating processed food, by just removing the added sugar and substituting starch, and without changing calories or weight. Can you imagine how much healthier they would have been if we hadn’t given them the starch?
This study establishes that all calories are not the same (“a calorie is not a calorie”); substituting starch for sugar improved these children’s metabolic health unrelated to calories or weight gain.

Give us NOT our daily bread with gluten!

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Unless you want to increase your risk of diabetes and probably many other diseases, according to this study (on mice):


Gluten-free diet reduces adiposity, inflammation and insulin resistance associated with the induction of PPAR-alpha and PPAR-gamma expression.

Quote:

Our data support the beneficial effects of gluten-free diets in reducing adiposity gain, inflammation and insulin resistance. The data suggests that diet gluten exclusion should be tested as a new dietary approach to prevent the development of obesity and metabolic disorders.

Comment:

More and more studies indicate deleterious effect of wheat consumption. The problem is not only in the very high concentration of carbohydrates, 60-80% by weight which is nearly as high as in pure sugar, but the presence of several other harmful compounds such as auto-immune triggering low molecular mass wheat proteins, nutrient-blocking lectins (agglutins), mood-altering addictive exorphins and other plant poisons.

NO THANKS!
 (Source: Wiki)

LDL cholesterol doesn't matter!

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According to this study (Framingham data):

Increased Small Low-Density Lipoprotein Particle Number

Compared with participants without the MetSyn [Metabolic Syndrome], those with the MetSyn had a higher CVD [Cardio Vascular Disease] event rate. However, among participants with the MetSyn, CVD rates were similar for groups with an elevated versus a lower number of small LDL particles (defined by the sex-specific median).

Conclusions— Small LDL particle number is elevated in the MetSyn, increases with the number of MetSyn components, and most prominently is correlated with triglycerides and HDL-C. Whereas increased small LDL particle number identified the MetSyn with high sensitivity, a higher small LDL particle number was not associated with greater CVD event rates in people with the MetSyn.

Putting it in simple terms: the common misconception that LDL correlates with cardio-vascular disease was caused by bad math! LDL correlated with MetSyn and MetSyn correlates with CVD.  Medical establishment leaders with insufficient mathematical training  incorrectly believed that correlation supposedly follows the "The law of syllogism"  (i.e. if LDL → MetSyn and MetSyn → CVD then LDL → CVD) - BUT IT DOES NOT!

 That study simply proved it by finding that in the sub-population of people who already had MetSyn, the number of small LDL particles did not matter!    Cholesterol theory is very dead and thoroughly debunked, case closed!  Fire them all and move on, next myth please...
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Bad science and politically motivated low fat dietary guidelines finally exposed and ditched!

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Recent (20/02/2015) New York Times article by Nina Teicholz (**):

The Government’s Bad Diet Advice

Quotes

First, last fall, experts on the committee that develops the country’s dietary guidelines acknowledged that they had ditched the low-fat diet. On Thursday, that committee’s report was released, with an even bigger change: It lifted the longstanding caps on dietary cholesterol, saying there was “no appreciable relationship” between dietary cholesterol and blood cholesterol.
...
Instead of accepting that this evidence was inadequate to give sound advice, strong-willed scientists overstated the significance of their studies.
Much of the epidemiological data underpinning the government’s dietary advice comes from studies run by Harvard’s school of public health. In 2011, directors of the National Institute of Statistical Sciences analyzed many of Harvard’s most important findings and found that they could not be reproduced in clinical trials.
...
In 2013, government advice to reduce salt intake (which remains in the current report) was contradicted by an authoritative Institute of Medicine study[*]. And several recent meta-analyses have cast serious doubt on whether saturated fats are linked to heart disease, as the dietary guidelines continue to assert.

Uncertain science should no longer guide our nutrition policy. Indeed, cutting fat and cholesterol, as Americans have conscientiously done, may have even worsened our health. In clearing our plates of meat, eggs and cheese (fat and protein), we ate more grains, pasta and starchy vegetables (carbohydrates). Over the past 50 years, we cut fat intake by 25 percent and increased carbohydrates by more than 30 percent, according to a new analysis of government data. Yet recent science has increasingly shown that a high-carb diet rich in sugar and refined grains increases the risk of obesity, diabetes and heart disease — much more so than a diet high in fat and cholesterol.

It’s not that health authorities weren’t warned. “They are not acting on the basis of scientific evidence, but on the basis of a plausible but untested idea,” Dr. Edward H. Ahrens Jr., a top specialist at Rockefeller University and prominent critic of the growing doctrine on dietary fats and cholesterol, cautioned back in the ’80s.
...
Since the very first nutritional guidelines to restrict saturated fat and cholesterol were released by the American Heart Association in 1961, Americans have been the subjects of a vast, uncontrolled diet experiment with disastrous consequences. We have to start looking more skeptically at epidemiological studies and rethinking nutrition policy from the ground up.
Until then, we would be wise to return to what worked better for previous generations: a diet that included fewer grains, less sugar and more animal foods like meat, full-fat dairy and eggs.

Other links:

*) She probably meant this report: Sodium Intake in Populations: Assessment of Evidence (14/05/2015)

**) Nina Teicholz, author of “The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet.”

http://stan-heretic.blogspot.ca/2015/02/useless-low-fat-dietary-guidelines-by.html

http://stan-heretic.blogspot.ca/2015/01/salt-intake-not-correlated-with.html

http://stan-heretic.blogspot.ca/2015/01/are-some-diets-mass-murder.html

http://stan-heretic.blogspot.ca/2013/05/dietary-fats-undeserved-bad-reputation.html

http://stan-heretic.blogspot.ca/2013/10/lesson-from-medical-history-beware-of.html



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Useless low fat dietary guidelines by governments, no scientific justification!

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Open Heart/BMJ just published a meta-study:

Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis

Objectives National dietary guidelines were introduced in 1977 and 1983, by the US and UK governments, respectively, with the ambition of reducing coronary heart disease (CHD) by reducing fat intake. ...

Conclusions

Dietary recommendations were introduced for 220 million US and 56 million UK citizens by 1983, in the absence of supporting evidence from RCTs.

Discussion
The main findings of the present meta-analysis of the six RCTs [Randomized Controlled Trials] available at the time of issuing dietary guidelines in the US and UK indicate that all-cause mortality was identical at 370 in the intervention and control groups. There was no statistically significant difference in deaths from CHD. The reductions in mean serum cholesterol levels were significantly higher in the intervention groups; this did not result in significant differences in CHD or all-cause mortality.
It is a widely held view that reductions in cholesterol are healthful per se. The original RCTs did not find any relationship between dietary fat intake and deaths from CHD or all-causes, despite significant reductions in cholesterol levels in the intervention and control groups. This undermines the role of serum cholesterol levels as an intermediary to the development of CHD and contravenes the theory that reducing dietary fat generally and saturated fat particularly potentiates a reduction in CHD.
...
There was best practice, randomised controlled trial, evidence available to the dietary committees, which was not considered and should have been. The results of the present meta-analysis support the hypothesis that the available RCTs did not support the introduction of dietary fat recommendations in order to reduce CHD risk or related mortality. Two recent publications have questioned the alleged relationship between saturated fat and CHD and called for dietary guidelines to be reconsidered.31 ,32 The present review concludes that dietary advice not merely needs review; it should not have been introduced.

Actual data from the publication:

References and links:

http://www.zoeharcombe.com/blog/

Interestingly, the original studies at that time produced similar similar conclusions of non-supporting the reduction of dietary fat.  The following quotes are from Zoë Harcombe's blog (one of the main author of the above quoted study):

The studies’ own conclusions.  These are the verbatim conclusions from each of the studies:

1965 Rose Corn and olive oil: “It is concluded that under the circumstances of this trial corn oil cannot be recommended as a treatment of ischaemic heart disease. It is most unlikely to be beneficial, and it is possibly harmful.” (ref 9)

1965 Research Committee Low-fat diet: “A low-fat diet has no place in the treatment of myocardial infarction” (ref 10) [heart attack].

1968 MRC soya-bean oil: “There is no evidence from the London trial that the relapse-rate in myocardial infarction is materially affected by the unsaturated fat content of the diet used.” (ref 11)

1969 Dayton LA Veterans study: “Total longevity was not affected favorably in any measurable or significant degree… For this reason, and because of the unresolved question concerning toxicity, we consider our own trial, with or without the support of other published data, to have fallen short of providing a definitive and final answer concerning dietary prevention of heart disease.” (ref 12)

1970 Leren Oslo Diet Heart study: “Epidemiological studies have demonstrated several factors associated with the risk of developing first manifestations of coronary heart disease. Blood lipids, blood pressure and cigarette smoking are such risk variables… In spite of the small numbers this observation lends some support to the view that the multi-factorial approach is the best way to the solution of the coronary heart disease problem.”(ref 13)

1978 Woodhill Sydney Diet Heart Study: “Survival was significantly better in the P [control] Group.” “It must be concluded that the lipid hypothesis has gained little support from secondary intervention studies.” (ref 14)
...

Just a spoonful of sugar (with CO2) helps the medicine go down

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http://en.wikipedia.org/wiki/Sugar

http://ajph.aphapublications.org/doi/abs/10.2105/AJPH.2014.302151

Quotes:

Objectives. We tested whether leukocyte telomere length maintenance, which underlies healthy cellular aging, provides a link between sugar-sweetened beverage (SSB) consumption and the risk of cardiometabolic disease.
...
Results. After adjustment for sociodemographic and health-related characteristics, sugar-sweetened soda consumption was associated with shorter telomeres (b = –0.010; 95% confidence interval [CI] = −0.020, −0.001; P = .04). Consumption of 100% fruit juice was marginally associated with longer telomeres (b = 0.016; 95% CI = −0.000, 0.033; P = .05). No significant associations were observed between consumption of diet sodas or noncarbonated SSBs and telomere length.
Conclusions. Regular consumption of sugar-sweetened sodas might influence metabolic disease development through accelerated cell aging. (Am J Public Health. Published online ahead of print October 16, 2014: e1–e7. doi:10.2105/AJPH.2014.302151)

Notice the lack of correlation for non-carbonated sugar-sweetened beverages!

More on the carbohydraty poison, today's news.  Skim milk anyone?

Quote:

In women the adjusted mortality hazard ratio for three or more glasses of milk a day compared with less than one glass a day was 1.93 (95% confidence interval 1.80 to 2.06). For every glass of milk, the adjusted hazard ratio of all cause mortality was 1.15 (1.13 to 1.17) in women and 1.03 (1.01 to 1.04) in men. For every glass of milk in women no reduction was observed in fracture risk with higher milk consumption for any fracture (1.02, 1.00 to 1.04) or for hip fracture (1.09, 1.05 to 1.13). The corresponding adjusted hazard ratios in men were 1.01 (0.99 to 1.03) and 1.03 (0.99 to 1.07). In subsamples of two additional cohorts, one in males and one in females, a positive association was seen between milk intake and both urine 8-iso-PGF2α (a biomarker of oxidative stress) and serum interleukin 6 (a main inflammatory biomarker).

Interestingly, detrimental effects seem to be related to the milk lactose contents rather than fat or proteins, because consumption of milk products that are high in fat and lower in lactose, such as fermented milk, cheese or cream, seem to correlate with more favorable biomarkers profile.

Comparing milk with other dairy products
Particularly noteworthy is that intake of fermented milk products such as yogurt and soured milk and cheese were associated with lower rates of fracture and mortality. Furthermore, we observed a positive association only between milk intake and markers of oxidative stress (urine 8-iso-PGF2α) and inflammation (serum interleukin 6). Previously, we found a negative relation between bone mineral density and 8-iso-PGF2α.42 63 Interleukin 6 seems to be causally related to cardiovascular disease64 and may influence bone loss and osteoporosis.65 Importantly, those who consume high amounts of non-fermented milk have a more non-favourable cardiovascular risk factor profile, with higher blood pressure, lower high density lipoprotein cholesterol levels, and higher insulin resistance.18 In contrast, intake of cheese and fermented milk products is related to higher high density lipoprotein cholesterol levels, less insulin resistance, and a lower risk of myocardial infarction.18 22 23 24 In addition, a recent small randomised cross over study indicated that the intake of a fermented dairy diet seemed to provide a more favourable biomarker profile than that of a non-fermented dairy diet.66

High carb and low caloric intake from fat and proteins may increase the risk of dementia in elderly!

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The title is a short version of the concluding sentence from a new Mayo Clinic study. The study tracked 937 initially healthy people aged 70-89 for 3.7 years. During this period 200 developed mild cognitive impairment (MCI) or dementia.

Those patients who were in the highest quartile (i.e. a group) of carbohydrate consumption (as percentage of total calories), have had approximately twice the risk of MCI or dementia (1.89 times, confidence interval P for trend =0.004(*)). Those who belonged to the highest quartile of fat consumption had about one-half the risk of developing MCI or dementia (0.56, P for trend = 0.03(**)). Those with the highest protein intake had 21% lower risk.

The fact that fat, especially saturated seems to be beneficial in dementia and other neurological degenerative diseases, has been known for some time, see for example the references in my past posts: this or this

This study however, is probably one of the first, if not the first, to concentrate on all three macronutrients' intake rather than some partial aspects of the diet.

Quote:

A dietary pattern with relatively high caloric intake from carbohydrates and low caloric intake from fat and proteins may increase the risk of MCI or dementia in elderly persons.

Although the full text is pay-walled, a short writeup is posted on the Mayo Clinic website.

Interestingly, a comparison between the highest quartile of total carbohydrates with the highest sugar (see the quote below), shows that the sugar impact was negative but not to the same extent as the total carbohydrate. This may be indicating that some other form of cabohydrate than the sugar alone, may be the most detrimental to the neurological health. Perhaps the total starch [ *** WHEAT?! ***] or just the total glycemic load?

Those who reported the highest carbohydrate intake at the beginning of the study were 1.9 times likelier to develop mild cognitive impairment than those with the lowest intake of carbohydrates. Participants with the highest sugar intake were 1.5 times likelier to experience mild cognitive impairment than those with the lowest levels.

But those whose diets were highest in fat - compared to the lowest - were 42 percent less likely to face cognitive impairment, and those who had the highest intake of protein had a reduced risk of 21 percent.

When total fat and protein intake were taken into account, people with the highest carbohydrate intake were 3.6 times likelier to develop mild cognitive impairment.

"A high carbohydrate intake could be bad for you because carbohydrates impact your glucose and insulin metabolism," Dr. Roberts says. "Sugar fuels the brain - so moderate intake is good. However, high levels of sugar may actually prevent the brain from using the sugar - similar to what we see with type 2 diabetes."

Wiki 

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Notes:
(*) It means that the probability of the result being by chance is 1/250.
(**) Probability of the result being by chance is 1/33.
(***) Added 13/01/2013, inspired by this .

(I am grateful and indebted to the best source of alerts about new interesting nutrition studies - vegan discussion groups!  Oh my oh my...  Thank you drmcdougall.com )
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Obesity not always tied to higher heart risk

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And lack of obesity is not a protection. The study confirms that obesity and metabolic syndrome are most likely unrelated causually, although may be coincidentally correlated to some extent.

A new UK study is discussed here.

Quote:

"People with good metabolic health are not at risk of future heart disease -- even if they are obese," Hamer told Reuters Health.

On the flip side, the non-obese in poor metabolic shape face as much risk as the unhealthy obese, the researchers concluded.

The findings, published in the Journal of Clinical Endocrinology & Metabolism, are based on more than 22,000 middle-aged participants in national health studies conducted in England and Scotland.

According to the researchers, the results suggest that metabolic factors may be more important in predicting a person's risk of cardiovascular disease than excess body weight in itself.