Obesity, Cholesterol and Death Rates - part 3 of 3


zoe_harcombe__150
by Zoë Harcombe
Author of Why do you overeat? When all you want is to be slim,
Stop Counting Calories & Start Losing Weight,
and The Obesity Epidemic: What caused it? How can we stop it?


Cholesterol and mortality - specific studies
The Honolulu Study(1) was a 20 year study of cholesterol levels and mortality in 3,572 Japanese American men. The study concluded that "Only the group with low cholesterol concentration at both examinations had a significant association with mortality". The authors went on "We have been unable to explain our results". (I.e. we were expecting lower cholesterol to equal lower mortality, not the other way round).

All credit to the team for their honest reporting of these unexpected results and their final statement in the abstract: "These data cast doubt on the scientific justification for lowering cholesterol to very low concentrations (<4·65 mmol/L) in elderly people."

Framingham similarly concluded that "There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels)."(2) Kendrick does a clever calculation on this quotation and translates this into - a reduction in cholesterol from 5 to 4 mmol/L would increase your risk of dying by 400%.

Elaine Meilahn reported in Circulation (2005) "In 1990, an NIH (National Institutes of Health) conference concluded from a meta-analysis of 19 studies that men and, to a lesser extent, women with a total serum cholesterol level below 4.2 mmol/L exhibited about a 10% to 20% excess total mortality compared with those with a cholesterol level between 4.2 and 5.2 mmol/L. Specifically, excess causes of death included cancer (primarily lung and hematopoietic), respiratory and digestive disease, violent death (suicide and trauma), and hemorrhagic stroke."(3)

Close
Back to - this is serious. The doctors' Hippocratic oath is "First do no harm". Surely we are doing real harm by lowering cholesterol levels? Not just to minds and muscles and quality of life of humans, but to the length of the life of those humans on statins.

This also says to me - even though saturated fat has nothing to do with cholesterol, it doesn't actually matter. Even if it did - cholesterol is only associated with CVD deaths in an inverse way. If fat did raise cholesterol - as public health officials like to claim - it could save lives! (Their words, not mine.)

Our global dietary advice was changed in 1977 in the US and 1983 in the UK as a result of a biased study of seven handpicked counties. Had the data been available for the 192 countries we can analyse now, or had Keys even considered all the data that was available to him at the time (for France etc), our conclusion may have been that we need to protect cholesterol levels in the body. We may have realised that the last thing we should be trying to do is lowering cholesterol - unless we're trying to lower life expectancy for some reason.

Zoë Harcombe
www.zoeharcombe.com
http://www.theobesityepidemic.org/

References
(1) Schatz, Masaki, Yano, Chen, Rodriguez and Curb, "Cholesterol and all-cause mortality in elderly people from the Honolulu heart programme", The Lancet, (August 2001).
(2)
Anderson, Castelli and Levy, "Cholesterol and Mortality: 30 years of follow-up from the Framingham Study", Journal of the American Medical Association (JAMA), (1987).
(3)
Elaine Meilahn, "Low serum cholesterol: Hazardous to health?" Circulation, (2005).
 


Post Script - A small technicality?

On p35 of The Great Cholesterol Con, Kendrick says: "How can eating saturated fat raise LDL levels? It is not merely biologically implausible, it is biologically impossible. Boy does that statement make me a hostage to fortune!"

I arranged to meet a biochemist at a local university to try to get to the bottom of this statement. The biochemist (who has more qualifications than I've had pork crackling) was sadly so brainwashed in the ‘fat is bad' theory that he just kept saying eating fat raises cholesterol.

When I asked him to talk me through the biochemical pathway from fat digestion through to how this impacts cholesterol he said he didn't know the digestive process well enough - we would need to add a dietician into the conversation.

This was alarming enough. I then said - we eat 39 grams of butter per person per week in the UK and about 1.4 kilos of flour - didn't he think it was more likely that the flour was making us fat and sick. He said it only took a drop of arsenic to kill us. I left shortly afterwards.

Is Kendrick right? LDL (remember this is not cholesterol - it is a low density lipoprotein) is the residue from IDL (intermediate density lipoprotein), which is the residue from VLDL (very low density lipoprotein). VLDL is one of the measures you get in your blood cholesterol test (actually they estimate it - they don't measure it - they only measure total cholesterol and HDL leaving two other unknowns in an equation with four variables and you thought this was scientific). (They also call VLDL 'triglyceride', which is confusing and unhelpful).

Cutting a complex story short (it is explained in my book in different passages), carbohydrates can impact VLDL levels (Acetyl-CoA being the start of the process by which the body makes cholesterol and part of the Kreb's cycle whereby the body turns glucose into Adenosine Tri-Phosphate, ATP), but I really have found no way in which the fat that we eat can do so.

Because fat is not water soluble, it is packaged into a lipoprotein in the digestive system. The lipoprotein that fat goes into is the biggest one - the chylomicron - and then it travels off into the body to go and do the essential repair and maintenance jobs that fat does. Does the fat say - hang on Mr chylomicron - we need to go via the liver and see if we can mess up the body's VLDL production in some way?!

Do ask this ‘how' question (in detail) of someone who thinks that this is possible. I am still open to someone answering this, but I'm not holding my breath.

Fructose, on the other hand, we do know goes straight to the liver to be metabolised. Could that, and other carbohydrates, impact VLDL production? The evidence I have already seen is strong that they do.

Zoë Harcombe
Her first book was published in 2004 "Why do you overeat? When all you want is to be slim". 
This was followed by "Stop Counting Calories & Start Losing Weight"
Her third book, "The Obesity Epidemic: What caused it? How can we stop it?", was published late in 2010. 
Zoe came across the cholesterol debate wondering why people had stopped eating real food (at precisely the time that obesity rates started to double and double again) and what fat had done to be so demonised and she discovered some other shocking errors along the way.

www.zoeharcombe.com
www.theobesityepidemic.org

February 2012


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