Why High Fat?
The most important take-home message is to only increase your fat intake once you lower your carbs. And remember it is healthy fat we want to increase such as avocado, butter, olive oil and coconut oil, not ‘fatty foods’, there is a difference.
If you increase your fat and don’t lower your carbs, all you are doing is ending up on the Standard American Diet (SAD) which is high-fat high carb, and the cause of all the modern health problems such as obesity, T2 diabetes, heart disease, stroke and cancer.
If you increase your fat but don’t cut back on the bread, cakes and biscuits, you are going to end up with weight gain, poor appetite and poor biomarkers, pretty much where you probably started off. This is the most critical step to get right.
Do not to go for low-fat products. When fat is removed, so is much of the nutrition and it is generally replaced with some form of carbohydrate. For example, low-fat cream cheese has 15% carbs whereas regular spreadable cream cheese has only 4%. You will go through a period of reading every label, but you will soon recognise the brands and the foods to buy.
Buy the least processed, freshest, closest to nature foods as you can. If it has a long expiry date, ask yourself why? Food shouldn’t last months or years, buy food that rots, buy food that your grandmother would recognise and buy ingredients, not products. Simple rules, simple food.
The fear of fat and cholesterol are the foundation of our dietary guidelines for the past 2 generations. It is wrong and there is no scientific basis (see links in the navigation bar for more articles). I encourage you to read these and learn how research regarding cholesterol has changed over the past decade.
This is a great low-carb lesson on all things cholesterol. It explains how cholesterol is essential to all humans and really it is not cholesterol which is the problem but the proteins that carry cholesterol around the body. The great visuals show LDL, LDL size, LDL particle count and the bottom line is that cholesterol is NOT the enemy.
I have embedded a clip at the bottom of this page for those who want to delve deeper, but here is a brilliant presentation by Dr Andreas Eenfeldt which brilliantly summarises the science behind LCHF and why we have got it wrong about reducing fat.
Another article by Professor Grant Schofield talks about how hard it is to challenge the establishment. My favourite quote in the article,
“science isn’t a democracy. We don’t have a vote and the most popular hypothesis wins. We deal with evidence”
For a full in-depth explanation of the relationship between carbs, lipoproteins and inflammatory factors HDL, LDL, triglycerides… read “The Art and Science of Low Carbohydrate Living” by Volek and Phinney. It explains the complex picture and relationship between carbs, fat, LDL, HDL, TG.
For decades we have been told to reduce our fat intake, especially saturated fats to reduce cholesterol and our risk of cardiovascular disease (CVD). Yes reducing saturated fats and butter etc from our diet reduces your cholesterol, but it mainly reduces HDL which is your good cholesterol and makes smaller LDL (bad cholesterol) which is more damaging.
The majority of cholesterol circulating in our bloodstream is low-density lipoprotein cholesterol (LDL). The proposed link between LDL and heart disease is the basis behind restricting cholesterol and saturated fat intake, and the use of statin medication. Studies have now shown you can indeed reduce LDL by dietary restrictions, or by the use of statins, but the reduction does not actually reduce the incidence of heart disease or reduce mortality rates.
“People have been recommending low-fat diets for 30 years, and then it turns out to be completely wrong! There is no proven correlation between saturated fats and CVD”. Fredrik Nyström, Professor of Internal Medicine, Linköping.
“It’s time to face the facts. There is no connection between saturated fats and CVD”. Peter Nilsson, Professor of Cardiovascular Research, Lund.
“Two generations of Swedes have been given bad dietary advice and have avoided fat for no reason. It’s time to rewrite the dietary guidelines and base them on modern science”. Göran Berglund, Professor of Internal Medicine, Lund.
LDL (bad) carries cholesterol and other lipids from the liver to the body and the organs.
HDL (good) carries cholesterol and lipids from the body back to the liver for disposal.
So too much LDL can lead to an accumulation in circulation, arterial walls, plaque formation and arterial disease – or is it? New studies have shown that reducing LDL by a low-fat diet or a high-fat diet, the high-fat diet does a better job at reducing the real incidence of heart disease. So much so, the Lyon Diet Heart Study was terminated early due to the dramatic decrease in mortality with the group that ate the 40% fat Mediterranean type diet vs. the American Heart Assoc Healthy Diet. Another study of postmenopausal women showed reducing dietary fat intake reduced LDL but had no effect on cardiovascular disease (stroke, heart attack, and overall mortality) after 8 years.
LDL quality vs quantity
It is also known that LDL is only part of the picture of lipid profiles. Smaller LDL particles are more atherogenic (dangerous) than larger ones. And yes LDL concentrations increase as a result of a low carb diet, BUT low carb diets significantly increase the LDL particle size and the compelling new data associates small LDL particles with increased rick of CVD.
Furthermore, you should not be concerned if on a low carb diet your LDL remains the same or slightly increases. IF other lipid and inflammatory markers dramatically improve, generally your small particle LDL decreases, serum triglycerides reduce and HDL increases. All potent factors which reduce your overall CVD risk.
Statins and low carb diets
If your LDL is raised, the standard protocol is to decrease dietary cholesterol and saturated fats and possibly begin taking a statin. There is no question that statins reduce LDL but new studies are indicating their effect to reduce CVD is due to their anti-inflammatory effect rather than reducing LDL.
It is a difficult decision to start using a statin drug. The benefit of the anti-inflammatory effect, against the major side effects of dementia, fatigue, muscle pain and increased risk of diabetes. New figures show that up to 87% of the patients taking statins may be unnecessary. This is something that needs to be discussed and researched further.
Volek and Phinney state that if lowering your LDL is your main goal, then a low-fat diet and a prescribed statin make sense BUT should just lowering your LDL be the correct aim?
A low carb diet, however, improves LDL particle size, raises HDL (good), reduces triglycerides, lowers insulin resistance, lowers inflammatory markers and lowers blood pressure.
Raised fasting triglycerides (TG) are a clear risk factor for heart disease, they also are an early sign of insulin resistance and your bodies inability to metabolize carbohydrates.
The body generally has 5g of glucose circulating, but an average meal may contain 100g carbs. Anyone who is insulin resistant will convert these excess carbs into fat (via de novo lipogenesis) rather than converting the excess glucose into glycogen (which is self-limiting). These are turned into triglycerides which if they are not released from the liver, will build up and cause fatty liver disease (hepatic stenosis).
TG containing saturated fats are associated with insulin resistance more than those TG containing essential fatty acids. It is simplistic to think the saturated fats we eat are to blame for insulin resistance and CVD. However, with insulin resistance, the liver readily converts carbs to fat and the main product is saturated fat!! When excess carbs are eaten, saturate fat VLDL particles are produced by the liver, which in circulation are converted to small particle LDL (remember the dangerous, reactive ones). Therefore a high saturated fat content in your TG is directly related to your carb intake!! and how well your body processes it.
This is the lipoprotein that takes the lipids from the body back to the liver for disposal. It is one of our best indicators for long-term cardiovascular health. HDL is the lipid scavenger.
HDL also increase the bioavailability of nitric oxide (important regulator of vascular function and blood pressure), is an antioxidant, anti-inflammatory, antithrombotic, all contributing to its anti-atherogenic properties.
The basic understanding that dietary intake of saturated fat and LDL levels, predict CVD is to say the least, questionable. The current model of reducing fat intake (and increased carbs) has a marked negative effect on TG and HDL.
The TG/HDL ratio is a broader assessment of risk and its relationship with insulin resistance, making it superior and more accurate than focussing on LDL.
How do we improve the TG/HDL ratio? By reducing carbs we improve all CVD risk factors
- decrease TG
- increase HDL
- increase LDL particle size
“low carbohydrate diets are unparalleled by any other lifestyle intervention or even drug treatment, and therefore represents the most powerful method to improve this ratio”.
The Cochrane Collaboration (a review of all studies published) came to the conclusion “… no significant evidence for concluding that dietary saturated fats are associated with an increased risk of CHD or CVD”.
“atherosclerosis is NOT a lipid mediated disease, atherosclerosis is a lipoprotein mediated disease”
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