Higher Blood Sugar and Insulin Raise the Odds of Dying

Insulin resistance and heart disease

We know that there are good reasons to believe that insulin resistance may be one of the main causes of heart disease, and possibly the most important cause. Heart disease itself is the leading killer in the U.S. Higher blood sugar and insulin raise the odds of dying — and this is true even when these numbers are only a bit above normal.

Insulin is the hormone that helps to control blood glucose (sugar) by rising when carbohydrates are ingested and glucose increases, causing cells to take up glucose from the blood. Insulin resistance is the condition in which insulin becomes less effective, is characteristic of type 2 diabetes, and is often seen in obesity, sedentary people, and smokers.

The EPIC-Norfolk study looked at over 4600 men, age 45 to 79, who had glycated hemoglobin measured, and then were followed for an average of about four years.(1)

The EPIC-Norfolk Study

Glycated hemoglobin, often referred to as HbA1c, is a measure of long-term blood glucose levels. When blood glucose rises, some of the glucose attaches permanently to the hemoglobin in red blood cells, and this lasts for the lifetime of the red blood cell, which is about 4 months. An average blood glucose value can be calculated from the HbA1c.

So what happens when you measure HbA1c in a group of men and then see who died? See the following chart.

hba1c mortality

 

The chart is based on data from the EPIC-Norfolk study (source) and shows that each 1% increase in HbA1c is associated with a 28% increased risk of death in any given time period.

This is death from any cause, not just heart disease.

The first two bars in the graph represent normal HbA1c — depending on whom you ask. The next three bars represent pre-diabetes to diabetes, which is above 5.7.(Ref.)

Two points here, besides the obvious increase in death rates:

1. Death rates rose even below the level of pre-diabetes or diabetes. Therefore you could be at higher risk even if your doctor doesn’t think your blood glucose or HbA1c is too high.

2. The increase in death rates was continuous. Any increase in HbA1c means a higher death rate. This points to causation, not just association.

The Helsinki Policemen Study

A number of other studies have looked at the association between blood glucose and death rates, the Helsinki Policemen Study being one of them.(2) In this study, the participants were given a 2-hour glucose tolerance test, in which the subject takes a glucose drink and has his blood drawn at 0, 1, and 2 hours. Glucose and insulin are measured.

 

insulin CHD

This chart shows the incidence of coronary heart disease over follow-up of up to 25 years. The measurements are men grouped by quintiles (fifths) of insulin. Greater insulin resistance means more insulin is produced for a given glucose load.

The greater the insulin, the greater the incidence of coronary artery disease.

Ivor Cummins has a nice write-up of the Helsinki Policemen Study, and he suggests that the results minimized the relation between insulin and heart disease. That’s because the study measured insulin only once, at the beginning, and many of the policemen would have gone on to develop insulin resistance in the following years, for example by gaining weight. Hence if insulin had been measured more often, we might even less heart disease among men who kept their early insulin sensitivity.

There’s little doubt in my mind that insulin resistance is a powerful, perhaps the most powerful, predictor of heart disease. Cholesterol and lipoproteins are red herrings that have little if anything to do with heart disease.

How do you get or keep good insulin sensitivity?

  1. Stay lean. Being overweight or obese is strongly associated with insulin resistance.
  2. Avoid refined carbohydrates like sugar and anything made with grains.
  3. Exercise, especially strength training, strongly promotes insulin sensitivity.
  4. Intermittent fasting. Eating all the time, as we’re encouraged to do, is an unhealthy practice.
  5. If you need further help, consider berberine or metformin — but if you put the four steps above into practice, you probably won’t need further help.

Other than the first step, staying lean, not much else is even talked about in the mainstream, which is all about avoiding “high cholesterol” and saturated fat, and taking toxic statins.

So to avoid heart disease, you need to be independent and ignore much of what you hear elsewhere.

PS: For more like this, check out my books Muscle Up, Stop the Clock, and Top Ten Reasons We’re Fat.

PPS: Check out my Supplements Buying Guide for Men.

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Leave a Comment:

11 comments
ted says July 13, 2016

Thanks PD. Do you know if beta amyloid forms in pancreas during type 2 diabetes, like in brain with alzheimers?

Reply
    P. D. Mangan says July 13, 2016

    Beta amyloid is exclusively made in neurons, as far as I’m aware.

    Reply
      ted says July 19, 2016

      Just read this – http://www.sciencedirect.com/science/article/pii/S0197458008003229
      Beta amyloid and hyperphosphorylated tau deposits in the pancreas in type 2 diabetes

      Also, http://www.ncbi.nlm.nih.gov/pubmed/25036708
      Autophagy defends pancreatic β cells from human islet amyloid polypeptide-induced toxicity.

      Reply
        ted says July 19, 2016

        Also this:
        http://www.the-scientist.com/?articles.view/articleNo/37769/title/Autophagy-s-Role-in-Alzheimer-s/
        Low autophagy leads to more intraneuronal amyloid beta accumulation, and less AB plaques outside the neuron. So possibly intracellular/intraneuronal accumulation does more damage than extracellular amyloid beta.

        Some thoughts – high carb diets increase insulin which reduces autophagy. Thus, more beta amyloid accumulates inside/outside pancrease beta cells as it is not cleared by autophagy. Over time, amyloid damages pancreatic beta cells, so pancreas cannot produce sufficient insulin, thus hyperglycemia (type 2 diabetes market) develops. That’s a theory on t2 diabetes now.

        What would be very interesting is to induce t2 diabetes in mice, and then confirm via autopsy that there are amyloid deposits inside/outside pancreatic beta cells. Then, put the remaining mice on low-carb/fasting &exercise until they no longer have t2 diabetes (via hbA1c or other diabetes measurement for mice), like Ten Naiman does with patients in his charts on Twitter.

        Once the diabetes in mice is reversed, then see via autopsy whether their amyloid within/outside pancreatic cells is cleared up.

        I suppose the same mechanism could be applied to Alzheimers, but t2 diabetes is easier to measure via blood glucose etc.

        What are your thoughts on this?

        Reply
          ted says July 19, 2016

          PS, by “That’s a theory on t2 diabetes now.” I mean just my theory

          Reply
          P. D. Mangan says July 19, 2016

          Thanks for those links, Ted, very interesting. I think your experiment idea makes a lot of sense. It’s been shown that losing even a small amount of fat from the pancreas can reverse diabetes, and it makes sense that amyloid could be involved. And of course it ties in with Alzheimer’s as “type 3 diabetes”.

          Reply
          ted says July 19, 2016

          http://www.ncbi.nlm.nih.gov/pubmed/15590663
          Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo.

          So curcumin reduces AB formation and dismantles plaque. I’ve read it may be better to inhale it through nose ir inject to blood, as it eaten it may not be absorbed properly.
          This is very interesting stuff, I think it could apply to both Alz and T2D amyloid. The depressing part is that the paper is from 2005, and in more than 10 years nothing has been done about it

          Reply
          Allan Folz says July 20, 2016

          Very interesting set of dots, Ted.

          Dennis, I like the comments here as much as the posts. As you may recall, I was quite worried when you changed the look, but so far so good. Congratulations and kudos.

          Reply
          P. D. Mangan says July 20, 2016

          Thanks, Allan.

          Reply
Allan Folz says July 14, 2016

Of course, “Stay lean. Being overweight or obese is strongly associated with insulin resistance” is classic ‘Begs the Question’ fallacy. Leanness is a result; not an action. The problem is compounded when the mainstream goes beyond the fallacy and deigns to offer advice for being lean, more often than not the result of their advice is the exact opposite of leanness.

Reply
Ole says July 15, 2016

Just came across this recent study, which indicates that there seems to be a link between gut microbiome imbalance and the development of type 2 diabetes.

http://www.nature.com/nature/journal/vaop/ncurrent/full/nature18646.html

Two specific bacteria strains, namely “Prevotella copri” and Bacteroides vulgatus have been identified to be responsible for the production of BCAAs (Branch chained amino acids) in the intestines. Humans can’t produce BCAAs, so until now, the origin of BCAAs in the bloodstream have been a bit of a mystery.

BCAA is very popular, especially among bodybuilders and atheltes. Even Dr. Mercola is a big fan of it.

In addition, there seems to be a link (although weak) between the use of BCAAs and the development of ALS.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3049458/

Reply
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