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Showing posts with label obesity. Show all posts
Showing posts with label obesity. Show all posts

Monday, May 20, 2013

Dietary Fats and Health - Lawrence

Dietary Fats and Health

Glen D. Lawrence*  Department of Chemistry and Biochemistry, Long Island University, Brooklyn, NY
 

Abstract

Although early studies showed that saturated fat diets with very low levels of PUFAs increase serum cholesterol, whereas other studies showed high serum cholesterol increased the risk of coronary artery disease (CAD), the evidence of dietary saturated fats increasing CAD or causing premature death was weak. Over the years, data revealed that dietary saturated fatty acids (SFAs) are not associated with CAD and other adverse health effects or at worst are weakly associated in some analyses when other contributing factors may be overlooked. Several recent analyses indicate that SFAs, particularly in dairy products and coconut oil, can improve health. The evidence of ω6 polyunsaturated fatty acids (PUFAs) promoting inflammation and augmenting many diseases continues to grow, whereas ω3 PUFAs seem to counter these adverse effects. The replacement of saturated fats in the diet with carbohydrates, especially sugars, has resulted in increased obesity and its associated health complications. Well-established mechanisms have been proposed for the adverse health effects of some alternative or replacement nutrients, such as simple carbohydrates and PUFAs. The focus on dietary manipulation of serum cholesterol may be moot in view of numerous other factors that increase the risk of heart disease. The adverse health effects that have been associated with saturated fats in the past are most likely due to factors other than SFAs, which are discussed here. This review calls for a rational reevaluation of existing dietary recommendations that focus on minimizing dietary SFAs, for which mechanisms for adverse health effects are lacking.
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Read the complete article from Advances in Nutrition here.

Sunday, March 24, 2013

http://www.zoeharcombe.com/2013/03/salt-awareness-week-10-things-to-be-aware-of/

Salt Awareness Week – 10 things to be aware of

March 11-17 2013 is “Salt Awareness Week” in the UK – what exactly might we like to be aware of?
Let’s get some definitions out of the way first. Salt can be unrefined or refined. Unrefined salt is also known as sea salt. Unrefined (sea) salt comes with many valuable minerals and natural elements. Refined salt is also known as table salt. This is made up of sodium and chloride. There are approximately 2.4g of sodium in 6g salt. This means that approximately 40% of salt is sodium. You’ll see sodium on food labels, rather than salt.

Here are 10 things that you may find interesting about salt…

1) Like every other government target, the salt dictat has no evidence base

The NHS wants us to eat “no more than 6g salt per day.” (Ref 1) (which equates to 2,400mg sodium). Why? I have no idea and nor does the NHS. Why not 7? Why not 5? Why have a target at all? Goodness only knows. Just like 5-a-day, 14/21 alcohol units, 20-30g saturated fat, 18g fibre – none of these precise targets has precise evidence.

The NHS web site is supposed to provide evidence for government policy. Here is “Salt – the facts” which opens with “Many of us in the UK eat too much salt. Too much salt can raise your blood pressure, which puts you at increased risk of health problems such as heart disease and stroke” and then it goes on to tell you how to cut your salt intake. I don’t know about you but I found those ‘facts’ quite underwhelming.

2) We need to consume salt (and potassium) or we die

We die without salt. It’s as simple as that. Unlike cholesterol, which is also utterly life vital, our body doesn’t make salt. The term “essential nutrient” in nutrition mean that it is essential that we consume the nutrient. Salt is thus an essential nutrient. Fortunately it is in the majority of real foods, including water, and so ingestion of this vital mineral is not difficult.

Potassium is another essential dietary mineral. The potassium/sodium balance, is absolutely critical to the overall functioning of every cell in the human body. If salt levels fall too low, a condition called Hyponatremia can develop, which can be fatal. (Ref 2)

3) Salt has nothing to do with obesity

The inclusion of salt in the Academy of Royal Colleges obesity report (Ref 3) was quite bizarre because salt has nothing directly to do with obesity. It has no calories, no macronutrients (no fat, no protein, no carbohydrate) and therefore cannot directly impact obesity.

There may be an indirect argument that salt could encourage people to eat things. However, I would argue that people may desire doughnuts or biscuits (combinations of flour, sugar and salt), but that they would be unlikely to crave, say, anchovies, unless salt deficient for some reason. I would then expect a salt-deprived person to stop consuming anchovies once any salt deficiency were corrected and not to binge on them. The ‘but for’ test therefore points to the refined carbohydrates, containing salt, being substances of desire and not salt per se.

4) CASH has it in for salt

A charity called Consensus Action on Salt and Health (CASH) exists purely to campaign against salt. As the web site says: “CASH was set up in 1996 as a response to the refusal of the Chief Medical Officer (CMO) to endorse the COMA recommendations to reduce salt intake.” (COMA stands for Committee On Medical Aspects of Food Policy).

The COMA report merely says (and I quote) “The panel recommends that the dietary intake of common salt should not be increased further and that consideration should be given to ways and means of decreasing it.”

The worst thing that the COMA report could say about salt was: “High salt intakes have frequently been linked with the prevalence of high blood pressure in communities but a mechanism whereby salt could lead to the development of essential hypertension has not been established.”

Hang on a second – so there are alleged “frequent links”, for which no evidence is presented and we don’t even know how salt could impact hypertension (high blood pressure)… (I’ll answer this for them in a minute – we’ve known how since Carl Von Voit’s work in 1860).

The COMA report continues “Cross-cultural studies show a statistical association between estimates of salt intake and the average blood pressure of a community but detailed investigations within a single community frequently fail to demonstrate such a relationship.” And CASH was set up because the CMO failed to take action against salt?!

5) ‘High’ blood pressure is in fact normal

If you look at figures 1 and 2 in this highly referenced article, the actual population normal/average blood pressure is 140/86. The European Society of Hypertension and the World Health Organisation both define blood pressure of 140/90 as the baseline for high blood pressure. So normal has been redefined as high. This enables drug companies to medicate many more people.

6) Salt can increase blood pressure, but so what?

There is a very simple mechanism by which salt can increase blood pressure (of which the COMA report didn’t seem to be aware). Salt provides sodium. The normal concentration of sodium in blood plasma is 136-145mM (mmol/Litre). One of the easiest ways for the body to maintain the concentration of sodium is to increase fluid levels if sodium rises. If we consume salty food, we want to drink more (that’s why bars put free bowls of peanuts on the counter) so step 1 is for the increased intake of sodium to lead to an increase in fluid intake. Step 2 means that the additional fluid is more likely to be retained because the body is back in sodium concentration equilibrium, albeit with more sodium and more water.

Water retention in the human body can raise blood pressure. However, there are three points to make here:

i) Raised blood pressure is a symptom. It’s not a problem per se. What the salt antagonists fail to provide is any evidence for a substantial and/or sustained increase in blood pressure as a direct result of any defined level of salt consumption.
ii) Salt opponents also fail to provide any direct causation between salt consumption and end point disease (e.g. heart disease) regardless of whether or not salt impacts blood pressure.
iii) A completely overlooked point is that any rise in water retention from consuming even a couple of grams of salt is incomparable to the impact of consuming 100g of carbohydrates – which we are encouraged to consume (a few times a day) in illogical parallel with the discouragement of salt intake.

We can store up to 500g of glycogen if we consume carbohydrates that are not used up for energy. We know that each gram of glycogen is accompanied by four grams of water. Hence we can gain 2.5kg (c. 5lb) overnight by consuming carbohydrates above human need. This is way more significant in terms of water retention and blood pressure than any impact of a couple of grams of salt – and yet carb consumption is recommended and salt consumption is demonised. Yet another example of our completely incomprehensible dietary advice.

7) Even if salt impacts blood pressure, and even if this matters, reducing salt intake substantially would have negligible impact

The 1994 COMA report (Ref 4) states: “Its [The review group] recommendation was to reduce salt consumption by an average of 3g/day. It has been estimated that this would reduce average systolic blood pressure by about 3.5mm Hg.” [systolic blood pressure is the first of the two numbers we get].
Gary Taubes noted the same in The Diet Delusion: “cutting our average salt intake in half, for instance, which is difficult to accomplish in the real world – will drop blood pressure by perhaps 4 to 5 mm Hg in hypertensives and 2 mm Hg in the rest of us.”

So, halve your salt intake and your blood pressure may go from 130/X to 127/X?

If you have ever had your blood pressure read frequently (while in hospital or getting ready for an operation or a baby), or if you have one of those blood pressure machines at home, you will know that you hardly ever get the same reading twice in a row. Even within a couple of minutes, your blood pressure can vary by more than a handful of points – more than the amount it could possibly change by if you managed to halve your salt intake.

8) CASH’s evidence on “Salt & Health” is completely lacking

For the seven years after its formation, Consensus Action on Salt & Health was relying upon the 1994 COMA report. Since 2003 they have relied upon a Scientific Advisory Committee on Nutrition (SACN) report, called “Salt and Health”. (Ref 5)

Feel free to read the 134 page document. The summary will give you the key elements. The summary opens by saying: “Increased blood pressure, or hypertension, is the most common outcome that has been associated with high levels of salt intake. Hypertension is a major risk factor in the development of cardiovascular disease. The relative risk of cardiovascular disease increases as blood pressure rises even within what is considered the normal range of blood pressure, indicating that large numbers of people are at risk.”

i.e. the most common (the only?) outcome that salt intake has been associated with is increased blood pressure. If there were any direct association between salt intake and any actual disease, it would have been claimed.

Increased blood pressure in turn is then claimed to be a “major risk factor in the development of cardiovascular disease.” I disagree. High blood pressure (BP) (even when properly defined as actual high BP and not normal BP i.e. 140/86) is a symptom, not a cause. This makes blood pressure a condition observed at the same time as heart disease and not a risk factor. (It is far more likely the opposite direction of causation – heart disease causes high blood pressure – hence the symptom).
Notwithstanding this – the argument against salt still boils down to – we think salt is associated with blood pressure and we think blood pressure causes heart disease. So, by inference, they want us to think that salt causes heart disease.

The jewel in the crown of the anti-salt lobbyists is “The International Study of Salt & Blood Pressure” (Intersalt Co-operative Research Group, 1988). This study collected data on 24-hour urinary sodium excretion and blood pressure of over 10,000 adults in 52 population samples from 32 countries. Associations (note, not causation) were found between sodium excretion and blood pressure readings – until the four populations with very low salt intakes were removed from the analysis and then any statistical significance disappeared. (That latter point about the statistical significance disappearing was the view of the SACN Salt and Health report to give credit for honesty – it wasn’t my playing with numbers that led to this finding.)

Dr David Brownstein’s book Salt your way to health noted the findings from the Intersalt study as follows: “Although there was a slight relationship between blood pressure and sodium excretion in INTERSALT, a ‘smoking gun’ could not be found. This study showed a mild decrease in blood pressure (3-6mmHg systolic and 0-3mmHg diastolic) when there was a dramatic decrease in salt excretion.”

9) There is no evidence that salt causes heart disease; there is evidence that low salt is associated with heart attacks

A study of approximately 3,000 hypertensive subjects (men with high blood pressure) found that there was a 430% increase in myocardial infarction (heart attack) in the group with the lowest salt intake versus the group with the highest salt intake. (Ref 6) Knowing how vital salt is for human health, this should not be surprising – low-sodium diets have been shown to cause multiple nutrient deficiencies, including nutrients vital for heart health (calcium, magnesium, potassium and B-vitamins). (Ref 7)
The SACN report concluded: “There are insufficient reliable data on long-term effects of salt on cardiovascular disease outcomes to reach clear conclusions.” Quite.

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p.s. The interesting twist to researching salt is that the motive for attacking this substance has not been as obvious as usual. The motive in the anti-fat movement is clear – it gives the ‘food’ industry the green light to make highly lucrative fake low-fat food. The motive in the anti-cholesterol movement is clear – it gives the drug industry the green light to make drugs worth tens of billions of dollars and ‘food’ companies can make spreads and other ‘cholesterol-lowering’ fake foods.

The common bad relationships between the ‘food’ industry and health campaigners can be found in the salt world. Check out p12 of the April 2012 Action on Salt annual report – the usual suspects from the ‘food’ industry are warmly thanked for their support.

Who gains by demonising salt? The lo-salt company clearly does. The founder of Consensus Action on Salt & Health, Professor Graham MacGregor, has personally done well out of founding the organisation. MacGregor is now chairman of action on salt. MacGregor is also chairman of the Blood Pressure Association. He sits on the board for the World Hypertension League and recently served as President of The British Hypertension Society. MacGregor was awarded 37th place on the Independent on Sunday’s list of people who have made Britain a “much, much better place.” (Ref 9) Salt has given MacGregor’s life purpose – I believe that he believes that salt is a bad thing. I also think that he is wrong.

As a final thought – have you heard of the expressions “salt of the earth” or “worth his/her salt”? We describe someone as the salt of the earth when they are as good and worthy as anyone can be. The word salary comes from the Latin word salarium and has the root sal or salt. In ancient Rome, salary meant the amount of money given to a Roman soldier to buy salt, which was an expensive but essential commodity. This explains the “worth his salt” expression. Our language is telling us the truth, our government is sadly not.


References
1) http://www.nhs.uk/Livewell/Goodfood/Pages/salt.aspx
2) http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001431/
3) http://www.aomrc.org.uk/about-us/news/item/doctors-unite-to-deliver-prescription-for-uk-obesity-epidemic.html
4) http://www.actiononsalt.org.uk/salthealth/Recommendations%20on%20salt/42491.pdf
5) http://www.sacn.gov.uk/pdfs/sacn_salt_final.pdf
6) Alderman “Low urinary sodium is associated with greater risk of myocardial infarction among treated hypertensive men.” Hypertension. 1995
7) Engstrom et al “Nutritional consequences of reducing sodium intake.” Ann. Intern. Med. 1983.
8) http://www.charity-commission.gov.uk/Accounts/Ends18/0001098818_AC_20100430_E_C.PDF
9) http://www.independent.co.uk/news/people/news/the-ios-happy-list-2012–the-100-7661358.html?action=gallery&ino=37
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Read the complete article here.
Another article here.

More data in the Salt Wars - Aug 14, 2014; http://www.medpagetoday.com/Cardiology/Hypertension/47203

An article by Marion Nestle - http://www.foodpolitics.com/2014/08/its-salt-arguments-again-new-research-arguments-over-public-health-recommendations-and-issues-of-conflicts-of-interest/

Sunday, October 9, 2011

Why small LDL particles are the #1 cause of heart disease in the US



Why small LDL particles are the #1 cause of heart disease in the US

Posted on by Dr. William Davis

Ask your doctor: What is the #1 cause of heart disease in the US?

Let’s put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol
Too much saturated fat
Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I’d tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

–Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

–In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here’s a 2006 review.

–Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to “cut fat and eat more healthy whole grains.” Conventional diet advice has therefore triggered an expllosion in small LDL particles.

–When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either “pattern B,” meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus “pattern A,” meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called “pattern A.”

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with “pattern B” small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat (“wheat belly”) to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet
 

About Dr. William Davis

Dr. Davis is Medical Director of the Track Your Plaque program and advocate of early heart disease prevention and reversal. He practices preventive cardiology in Milwaukee, Wisconsin.