Diabetes Disaster in China

Diabetes

A new study shows that 11.6 percent of Chinese adults have diabetes.

“Diabetes in China has become a catastrophe,” said Paul Zimmet, honorary president of the International Diabetes Federation […] “The booming economy in China has brought with it a medical problem which could bankrupt the health system. The big question is the capacity in China to deal with a health problem of such magnitude.”

Bloomberg: China ‘Catastrophe’ Hits 114 Million as Diabetes Spreads

China is already worse off than the US where diabetes prevalence is about 11.3 percent. But it’s just the beginning. This is happening fast as China is modernizing and Chinese people are getting access to unlimited amounts of Western junk food, including sugar and rapidly digested starches.

Chinese people are getting diabetes at much lower weight than Western people. And the study shows more ominous statistics: In addition to the 11.6 percent with diabetes, another 50.1 percent has pre-diabetes.

Among young Chinese adults aged 18-29 about 40 percent has pre-diabetes and are on the verge of getting the disease. Thus one in four young Chinese adults risk a future of diabetes complications like early heart disease, blindness, dialysis and amputations.

This is not a problem for the health system. There’s no antidote to unlimited amounts of the poison causing this epidemic. The problem that needs to be fixed is in the food supply.

More

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Surprise: More Sugar, More Diabetes

The Doctor Asked: “What Have You Done?”

Dr Attia at TEDMED: What if We’re Wrong About Diabetes?

Failed Attempt to Cure Diabetes at Subway

Nearly 1 in 4 U.S. Teens Has Diabetes or Prediabetes!

All about diabetes

63 comments

Top comments

  1. Kim
    I'm sure T. Colin Campbell will blame it on meat or fish consumption.
    Read more →
  2. FrankG
    Once you realise that Type 2 Diabetes is not caused by obesity but that both are symptoms of the same underlying Metabolic Disorder, it then becomes reasonable to expect that different body types may display those symptoms in different ways.

    For example it seems significant if the excess fat mass is being stored just under the skin (subcutaneous), or in and around the internal organs (visceral). The latter is obviously less visible but more deleterious to health.

    The Asian phenotype seems to lend itself more to the visceral fat storage while still presenting as outwardly "lean".. so the metabolic damage may go unnoticed until it is too late.

    Of course these are generalisations and do not readily apply to the individual but rather at the population level; which is where these statistics are derived.

    Read more →
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All comments

  1. Paul
    correction: "...will kill you for it". Although you are only a messenger I suggest you run for your life troll.
  2. Z.M.
    Richard: "Some of favorite studies demonstrating the harmful effects of SFA"

    Selective citation at its finest. Whether saturated fat decreases LDL receptor activity or not is irrelevant because it does not change the fact that there is very little evidence that saturated fat is harmful.

    Richard: "http://www.ncbi.nlm.nih.gov/pubmed/16674358"

    A paper by Evan A. Stein, a guy with extensive ties to the pharmaceutical industry. He cited 7 studies in an attempt to support his case and only one of them found any meaningful benefit in CHD and total mortality and none of small benefits seen in these trials can actually be attributed to lowered cholesterol. He also cited two statin trials (woscops and care) which contradicted the whole "lower is better" idea.

    Richard: "http://www.ncbi.nlm.nih.gov/pubmed/22492369?dopt=Abstract"

    Selectively cited short term study. The majority of these short term studies find no increases in inflammation due to saturated fat and in fact some find that some inflammatory markers tended to decrease on the saturated fat diet. The so called short term benefits of these omega-6 oils may be due to its vitamin E content because vitamin E has been found to be anti-inflammatory in many short term trials.

  3. Galina L.
    Is it not it in the history of LCarbing in Sweden , that a court experts went through all studies results presented by the opponents of a doctor which treated her diabetic patients with LC diets , that supposed to prove that low-fat diets were unhealthy, and finding all their prove was not valid? It looks like Richard is trying to re-try the case.
    Reply: #57
  4. François
    I could not resist downloading all the "proof articles" that our vegan friends have cited. Not only the abstracts but the actual articles (I have access to a medical library and can download any article to take a look at the tables and at the whole articles, not only the summary. And Oh surprise, there is a lot more than what they have said. In nearly all the articles, when one looks at the tables (not at the conclusion), one sees that the "p" value of the above cited studies are not significant (ie they have no right to make any conclusions as they mean nothing statistically) and one also sees that the 95% confidence intervals overlap so dramatically that the difference between what is studied means nothing. Strange Richard Lowfat4ever and HealthyLongevity - if they are different people - omitted to state this. Maybe they do not know how to read statistics and can only gulp abstracts that fit their way of thinking... It is one thing to gargle oneself with complicated words like ""The findings from this meta-regression study are supported by other recent findings from mendelian randomization studies". It is another to read the tables correctly.

    In many of the articles cited as being the ultimate proof that cholesterol and saturated fats are "horrible for your health", there were follow-up articles or letters to the editor pointing that there were many errors in the articles or that some things had been overlooked (for example in the eskimo study, authors did not take into account the fact that the carbohydrate intake of eskimos at the time of the study, basically non existent on their traditional diet, was much higher bringing inflammation and oxydative stress. Strange that Richard Lowfat4ever omitted to speak of this important piece of information. I tell you, I'm quite sure his name is Keys and his grandfather Ancel!)

    In a follow-up letter to the editor after the Eskimo study, Dr Can did a remarquable job of looking at ALL the research done on Eskimos from an historical point of view. He noted:"As pointed out by Ebbesson et al., four decades ago coronary atherosclerosis was almost non-existent in Eskimos and the prevalence of diabetes mellitus (DM) was <0.4%[2,6]. In 1994, the prevalence of CHD was found to be 14% in Alaskan Eskimos aged 25 years or over [7]... Adoption of a higher carbohydrate diet was temporally associated with increasing CHD and DM incidence. Therefore, I hypothesize that by changing to a higher carbohydrate diet, Eskimos have increasing prevalence of DM and CHD... And From Ebbesson’s studies, I can conclude that Eskimos are or are used to be spontaneous lower carbohydrate eaters.

    Dietary counseling to increase the consumption of native Eskimo (lower carbohydrate) food was effective in reducing diastolic blood pressure, the plasma concentrations of total cholesterol, low-density lipoprotein cholesterol and improving glucose tolerance in Eskimos"

    Now, a little more about p values and confidence intervals. This piece of info is important because it is often the "forgotten piece" in the conclusions. For those who do not know what are either p values or confidence intervals, bear with me...

    I modified the following p-value explanation from Amazon Askville : Can you explain the concept of "p-value" to me in simple English?

    One of the unknown facts about biostatistics is that it's actually almost impossible to prove anything true. But it is strangely possible to prove that something is false. So instead of proving our hypothesis, we try to prove that all of the alternatives are wrong. We call that alternative the "null hypothesis".

    The p-value is the probability that your null hypothesis is correct. How to compute the p-value is beyond this explanation. In most studies, the chosen p-value is most often arbitrarily set at .05. That is, if the data show that the null hypothesis has less than a 5% chance of being right, we say it's wrong. That doesn't necessarily mean that our theory is right, but that's closest we can get statistically to « prove » something. Which is not entirely true, but it puts the burden of proof on somebody else who says that their theory is better, because we can at least show that the null hypothesis is not right.

    So anything that has a p-value greater than 0.05 means that it is statistically impossible to state that the point being made is true. But authors often forget to state this in their conclusions. How strange! Most of what our friends have cited have p-values MUCH higher than 0.05.

    Confidence intervals now. They are a way to statistically find the range of data looking at the same questions with a different sample of people. The bigger the sample and the smaller the confidence interval. A 95% confidence interval means that we are 95% confident that with a different set of data, the results would fall between the confidence interval upper and lower values. A quick way to compare data presented in a bar graph is to look at the confidence intervals. If they are completely different, there is a statistical difference. If they overlap by 25% or more, they are probably identical. If they overlap by less than 25%, you cannot say and you have to run statistical tests to find out. It so happens that the confidence intervals of the studies cited by our « friends » have massively overlapping confidence intervals. But why state such petty fact?

  5. Richard lowfat4ever
    ZM,

    you let yourself go too easily. The last study I recited, did not just look at the levels of inflammation but fatty liver as well. Saturated fat made the control group prone to fatty liver. In regards to Evan Stein, it's very easy us for to accept that "lower is better". Brown & Goldstein demonstrated with cell cultures that the physiologic LDL cholesterol for humans is the same that it is for other free-ranging mammalians that do not develop CHD, exceedingly low that is. Our physiology is designed by evolution to function optimally under very low cholesterol levels. Moreover, there are several studies that have established a strong link between dietary saturated fat consumption and carotid-intima media thickness.

    You seem to also have missed the three studies published this year that reported the strong association with increased risk of strokes, MI and mortality and serum saturated fat concentrations. See my previous post!

    Francois,

    denialists often write letters to the editor in regards to SFA & cholesterol studies. Bertelsen concluded in regards to the Eskimo's in 1940:

    "arteriosclerosis and degeneration of the myocardium are quite common conditions among the Inuit, in particular considering the low mean age of the population".

    The eskimo's carried tons of parasites potentially affecting beneficially to their lipid metabolism, nevertheless, in 1904, Bertelsen proved the existence of cancer in the native Inuit, diagnosing a case of breast cancer. During the following decades researchers documented that the existence of cancer was exceedingly common among the Inuit despite their relatively short life expectancy.Consistent with Bertelsen’s findings, an Inuit predating western contact who was mummified in approximately 1475, 450km north of the Arctic Circle was shown to have evidence of cancer, likely of the breast. It has also been documented that numerous preserved pre-contact Inuit who were mummified dating all the way back to 1,500 years ago had a severe degree of atherosclerosis, osteoporosis, and osteoarthritis, consistent with studies of Inuit living in the 20th century. Other evidence of poor health among the pre-contact Inuit includes iron deficiency anemia, trauma, infection, dental pathology, and children with downs syndrome and Perthes disease.

    See HealthyL's blog:
    http://healthylongevity.blogspot.fi/2012/08/forks-over-knives-and-hea...

    http://www.ncbi.nlm.nih.gov/pubmed/20320248
    http://www.ncbi.nlm.nih.gov/pubmed/14246293
    http://www.ncbi.nlm.nih.gov/pubmed/4412233
    http://www.ncbi.nlm.nih.gov/pubmed/8298320
    http://www.ncbi.nlm.nih.gov/pubmed/13448947

    Low incidence of cardiovascular disease among the Inuit--what is the evidence?
    http://www.ncbi.nlm.nih.gov/pubmed/12535749

    BTW, this is what Ancel Keys said about the Inuits:

    ”The fact is that nothing is really known about the incidence of atherosclerosis and coronary heart disease among Eskimos. According to Ehrström, arteriosclerosis is common among them, reaching an incidence of 29% in North Greenland, but the evidence is dubious, particularly in regard to atherosclerotic heart disease. In any case we could not expect a high incidence of coronary heart disease among primitive Eskimos because few of them attain an age when they would be likely victim of the disease. The majority of Eskimos no longer eat a high-fat diet, and of those who adhere to the old way of life probably not more than a total of 100 or so men are beyond the age of 50, though estimates are difficult in a widely dispersed population who do not know their own ages and are notorious for appearing far older than their years.”

    Replies: #56, #62
  6. FrankG
    So how am I and apparently many others, doing so very well -- by every measured test which the doctors can devise -- on a diet high in saturated animals fats which, according to all your "research", should be killing me?
    Reply: #58
  7. FrankG
    Galina L -- it was not a court hearing but (probably more importantly) the National Swedish Board of Health and Welfare did an investigation into LCHF after two dietitians reported Dr. Annika Dahlqvist...

    "The story of the rise of LCHF in Sweden is fascinating, and is one of those great examples of a single person making a real difference. Dr. Annika Dahlqvist is credited with starting the revolution around 2004. Dr. Dahlqvist had experienced success herself on the diet, with normalized weight and improvements in her health, and had started using the diet with patients in her medical practice, as well as starting a blog about the science and her experiences. Dr. Dahlqvist's influence might have remained fairly quiet and limited, but she was catapulted into prominence when two dieticians in Sweden reported her to the National Swedish Board of Health and Welfare. They were hoping to get Dr. Dahlqvist to be ordered to stop advising her patients to reduce carbohydrates in their diet, or even thrown out of the medical profession for her "sin". What happened instead was quite remarkable! The Board took the complaint seriously and did an investigation of the science of carbohydrate reduction in the diet. When they reached their conclusions in 2008, it was the opposite of what the dieticians had hoped: the board put out a report stating that treating patients with a low-carb high-fat diet was well-supported by science. This report was well-publicized in the media, and that's when LCHF in Sweden really started to take off."

    http://lowcarbdiets.about.com/b/2012/01/19/is-sweden-leading-other-co...

    Oh noes! So much for Ricky's "consensus of health authorities" :-P

  8. Paul
    Hear, hear. C'mon Richard show us your and your team's mental stamina ! - why my blood work and overall health after 7 years on LCHF is exemplary?.
  9. Galina L.
    Thank you, Frank. I will bookmark the link you sent to me To my amazement, when I googled "The history of low-carbohydrate diet in Sweden" in order to refresh the story in my memory before commenting, things like "Time to Retire the Low-Carb Diet Fad - Ellen Ruppel Shell" and "Are Low-Carb Diets Killing Sweden?" started to pop-up. It looks like the people who want to push everybody back into counting calories and living in a miserable and unhealthy state are making enough noise to spam-up Google.
    Reply: #60
  10. FrankG
    You are very welcome Galina. There is indeed plenty of "spam" trying to reverse the LCHF trend and you don't have to look too far to see the money trail... unfortunately for them and their vested interests (fortunately for our health) the genie has already been let out of the bottle and I don't think it is going back in :-)
  11. Z.M.
    Richard: "Saturated fat made the control group prone to fatty liver"

    Translation: Saturated fat did not actually cause fatty liver but since I believe saturated fat to be evil I'll add the word "prone" to exaggerate the results.

    The actual conclusion of the study: "In conclusion, compared with SFAs, dietary n-6 PUFAs reduce liver fat in overweight individuals in the absence of weight loss"

    In a short term study that failed to standardize the diets and vitamin E intake the reduction in liver fat in the n-6 group can't even be attributed to n-6 fats per se. Anyone citing this study as evidence against saturated fat is simply desperate.

  12. Paul
    Pharma-Troll, any comments on these two papers?, as you know liver is a pretty damn important organ.

    1)
    http://ebm.sagepub.com/content/238/2/151

    2)Dietary Saturated Fat Reduces Alcoholic Hepatotoxicity in Rats by Altering Fatty Acid Metabolism and Membrane Composition1,2
    Martin J. J. Ronis,*†3 Soheila Korourian,** Michelle Zipperman,* Reza Hakkak,‡ and Thomas M. Badger*††
    *Arkansas Children’s Nutrition Center and †Department of Pharmacology/Toxicology, **Department of Pathology, ‡Department of Dietetics & Nutrition, and ††Department of Physiology/Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR 72205
    ABSTRACT Rats fed a saturated fat diet are protected from experimentally induced alcoholic liver disease, but the molecular mechanisms underlying this phenomenon remain in dispute. We fed male Sprague-Dawley rats intragastrically by total enteral nutrition using diets with or without ethanol. In 1 control and 1 ethanol group, the dietary fat was corn oil at a level of 45% of total energy. In other groups, saturated fat [18:82 ratio of beef tallow:medium-chain triglyceride (MCT) oil] was substituted for corn oil at levels of 10, 20, and 30% of total energy, while keeping the total energy from fat at 45%. After 70 d, liver pathology, serum alanine aminotransferase (ALT), biochemical markers of oxidative stress, liver fatty acid composition, cytochrome P450 2E1 (CYP2E1) expression and activity and cytochrome P450 4A (CYP4A) expression were assessed. In rats fed the corn oil plus ethanol diet, hepatotoxicity was accompanied by oxidative stress. As dietary saturated fat content increased, all measures of hepatic pathology and oxidative stress were progressively reduced, including steatosis (P

  13. Eric Anderson
    What does a study include or exclude as a saturated fat? Is the study looking at cream, butter, tallow, and lard and excluding seed and nut oils like canola, corn, soy etcetera? How long is the study?

    For example when quick weight loss happens the first response may show great lipid blood work followed by a few months of higher blood lipid levels that then revert to the great or more optimal blood lipid levels associated with LCHF diets.

    The results from the NuSi diet studies may demonstrate the delta of the SAD 50% of calories from carbohydrate modern diet versus 5% or less of calories from carbohydrates. Let the evidence speak for itself.

    However, I suspect that some are so attached to a vegan world view that no matter the evidence they will still espose a vegan diet.

    I say "Let them eat wheat and sugar"

    The question is what blood profiles for glucose, Insulin, and ketones emerge from an 80% Carbohydrate, 50% Carbohydrate, or 5% carbohydrate diet.

    Even low glycemic carbohydrates at 50 to 80% of calories will elevate blood glucose and insulin levels as opposed to a 5% carbohydrate diet.

    Eric

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