The oils and fats that you eat do not make you fat or clog your arteries, or cause heart disease. This is one of the biggest health-related myths of all time. Scientists who study this subject have known the truth about fats for several years but such knowledge has barely percolated through to the general public.
More to the point, a high-fat diet is absolutely essential for good health, avoiding obesity and living longer. By appreciating and understanding this truth you will be much better equipped to optimize your health and extend your lifespan.
When we eat fats (any kinds of oils and fats) the digestive system breaks such fats down to smaller components that the body can handle. The fats go through various stages while being digested. Eventually most of the fats digested are converted into triglycerides and go into the blood stream as such. These triglycerides are wrapped up in protein wrappers (called lipoproteins) for transportation throughout the bloodstream to all parts of the body.
We need to understand that fat is a structurally integral part of every single cell membrane in our bodies. To repeat: Fat is structurally essential in EVERY SINGLE CELL in our bodies. So those triglycerides that we just mentioned (the end product of digesting fat) are fed by the bloodstream to all our body cells.
Fats (i.e. triglycerides) are required for many vital functions. Here are just some of those functions:
These are just 6 of the many health benefits of a diet high in healthy fats. But you may be wondering why fats don’t end up as surplus body fat?
The answer is that when fats go into the bloodstream as triglycerides for distribution around the body, they get used by body cells everywhere (in many different biological ways) instead of being stored as surplus body fat. But this begs a question: what about the triglycerides that get delivered to fat cells? Don't these triglycerides end up being stored as body fat?
The answer is yes, some of the triglycerides arising from fat consumption do indeed end up as stored-body fat inside fat cells, and this is why the myth that fat is fattening persists. But there are three considerations:
For these three reasons, fat consumption does not make you fat. So how do you get fat? You get fat by consuming sugary foods and processed carbs. These foods galvanize hormones that convert such foods into triglycerides (a well known process called 'lipogenesis') that are then stored as visceral fat.
When you consume sugary foods and processed carbs they make your glucose shoot up. This in turn makes insulin go up to bring down the level of glucose, and then store such glucose as visceral fat. The glucose is fully converted into fat and then stored.
Furthermore, the hormone insulin is 'programmed' to store glucose in fat cells located in visceral fat. Insulin is compelled to bring down blood glucose quickly, so the glucose is stored in visceral fat cells as fat because it offers a quick and easy place to store fat. This is the body's biggest reservoir of fat storage offering an immediate 'home' for the excess glucose in the blood. This is what the body is designed to do.
Sugary foods and processed carbs are also high in fructose since many foods and drinks contain added fructose. Unlike glucose, fructose does not trigger an insulin response, but even so it is much more fattening than glucose.
As explained in another part of this book, added fructose is truly your enemy number one in terms of the diet because it overwhelm the liver, forcing the liver to get rid of fructose by converting it into triglycerides which are then stored as visceral fat. Remember that regular sugar is half glucose and half fructose.
If you under-eat fat, you can become seriously ill (not to say obese) and eventually this can be fatal. If you over-eat fat (but avoid sugary foods and processed carbs), the stored fat will eventually be released as free fatty acids for fuelling our metabolic functions. However much fat you may consume, it will not make you put on weight provided you avoid sugary foods and processed carbs.
To clarify this vital point further, if you eat oils/fat with a sugary food (or with a processed carbohydrate), the sugar/carbs that you eat will make the body store more of the dietary fat than otherwise, thus making fat cells store more fat than the amount they release. So never combine dietary fat with dietary sugar/carbs. If you must consume sugar/carbs, avoid or minimize oils/fat in the same meal. And vice-versa: when you consume a high-fat meal, minimize or avoid sugar/carbs.
Providing you avoid (in the same meal) the consumption of sugar/carbs, the actual fat that you eat will not be fattening and will not end up as surplus body fat. The problem is that many high-fat foods are combined with sugar/carbs, such as pastries, bread & butter, waffles, chocolate, cookies, and many processed foods contain both fat and sugar in one form or another. These are fattening foods because of their sugar/carb content, not because of their fat content.
You are not being urged to follow a high-fat low-carb diet such as the Atkins diet. This is fatal because the high content of animal protein in such diets is very unhealthy.
Furthermore, 'atkins-type' diets typically include a high consumption of heated (i.e. unhealthy) fats that cause illness.
Rather, you are being urged to follow a high-fat, high-carb diet. But such carbs must exclude sugary foods and processed carbs. There are many high-carb foods that are super healthy and will not make you fat such as beans, lentils, sweet potatoes and many other legumes and starchy vegetables.
Also, a high-fat diet must exclude unhealthy fats such as processed polyunsaturated oils, all kinds of fat spreads and margarines, and any oils or fats that have been heated. Healthy fats include steam rendered lard, and good-quality organic cream, butter & cheese. Salad dressings made with extra-virgin olive oil that has been refrigerated is non fattening and healthy. Other examples of healthy fats include coconut oil, palm oil and other nut/seed oils providing they are cold-pressed, have not been heated at any point and have been refrigerated at all times from factory to mouth.
An argument that is usually put forward by those who favour low-fat diets (or the avoidance of saturated fat) goes like this: "saturated fat makes your VLDL and LDL cholesterol go up and this is bad for health". Well guess what, this is total baloney! Saturated fat has a zero harmful impact on VLDL and LDL cholesterol levels in the body.
This is so because it has been shown time and again in countless studies that dietary fat has no impact on blood cholesterol levels. Even foods high in cholesterol have no impact on blood cholesterol levels. Furthermore, a high level of blood cholesterol is healthy and not conducive to heart disease.
All the recent research shows that "eating fat significantly lowers VLDL cholesterol and has no impact at all on LDL in the blood, [thus greatly protecting against clogged arteries and heart disease]". Abridged extract from the book The Great Cholesterol Con, by Malcom Kendrick, ISBN: 1844546101.
To summarize, the oils and fats that we eat do not end up as surplus body fat and do not clog arteries or cause heart disease. This does not mean that you can eat oil/fat with great abandon! Think of oils and fats as condiments for adding to your food. Moderation in all things is a wise saying.
The so-called 'good fats' are super-healthy and indeed essential for losing weight and avoiding heart disease - they should be consumed daily in generous but not excessive amounts. The so-called 'bad fats' may not be fattening but they can cause cancer, heart disease and other serious illnesses and should be completely avoided.
The best possible diet for human biology is a high-fat, high-carb diet so long as you avoid sugary foods, processed carbs & unhealthy fats. There is a world of difference between good fats and bad fats, and knowing the difference is life-saving knowledge that will greatly improve your well-being and help you live longer.
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The takeaway message: follow a high-fat diet for optimum health and longevity, but avoid unhealthy fats (know the difference).
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Throughout this book we talk about optimizing health so as to extend life and remain healthy. But why exactly does better health help you live longer? Put another way, what exactly makes the body grow old and die?
The answer in a word is "telomeres". This is the holy grail for some longevity scientists. Inside the nucleus of a cell, our genes are arranged along twisted, double-stranded molecules of DNA called chromosomes. At the ends of the chromosomes are stretches of DNA called telomeres, which protect our genetic data, make it possible for cells to divide, and hold some secrets to how we age and get cancer.
Telomeres have been compared with the plastic tips on shoelaces, because they keep chromosome ends from fraying and sticking to each other, which would destroy or scramble an organism's genetic information.
Yet, each time a cell divides, the telomeres get shorter. When they get too short, the cell can no longer divide; it becomes inactive or "senescent" or it dies. This shortening process is associated with aging, cancer, and a higher risk of death. So telomeres have also been compared with a bomb fuse because once the telomere gets too short the body cell no longer divides and dies.
In white blood cells, the length of telomeres ranges from 8,000 base pairs in newborns to 3,000 base pairs in adults and as low as 1,500 in elderly people. (An entire chromosome has about 150 million base pairs.) Each time it divides, an average cell loses 30 to 200 base pairs from the ends of its telomeres.
Cells can normally divide only about 50 to 70 times, with telomeres getting progressively shorter until the cells become senescent or die.
Telomeres do not shorten in tissues where cells do not continually divide, such as heart muscle.
Without telomeres, the main part of the chromosome — the part with genes essential for life — would get shorter each time a cell divides. So telomeres allow cells to divide without losing genes. Cell division is necessary for growing new skin, blood, bone, and other cells.
Without telomeres, chromosome ends could fuse together and corrupt the cell's genetic blueprint, possibly causing malfunction, cancer, or cell death. Because broken DNA is dangerous, a cell has the ability to sense and repair chromosome damage. Without telomeres, the ends of chromosomes would look like broken DNA, and the cell would try to fix something that wasn't broken. That also would make them stop dividing and eventually die.
An enzyme named telomerase adds bases to the ends of telomeres. In young cells, telomerase keeps telomeres from wearing down too much. But as cells divide repeatedly, there is not enough telomerase, so the telomeres grow shorter and the cells age.
As a cell begins to become cancerous, it divides more often, and its telomeres become very short. If its telomeres get too short, the cell may die. But very often these cells escape death by making more telomerase enzyme, which prevents the telomeres from getting even shorter.
Too much telomerase can help confer immortality onto cancer cells and actually increase the likelihood of cancer, whereas too little telomerase can also increase cancer by depleting the healthy regenerative potential of the body. To reduce the risk of cancer we need an ideal level of telomerase, with not a whole lot of room for error.
This clarifies that “telomerase shots” are not the magical anti-aging potion that Faust and so many other humans have sought throughout history.
Many cancers have shortened telomeres, including pancreatic, bone, prostate, bladder, lung, kidney, and head and neck.
Measuring telomerase may be a way to detect cancer. And if scientists can learn how to stop telomerase, they might be able to fight cancer by making cancer cells age and die. In one experiment, researchers blocked telomerase activity in human breast and prostate cancer cells growing in the laboratory, prompting the tumour cells to die. But there are risks. Blocking telomerase could impair fertility, wound healing, and the production of blood cells & immune-system cells.
Geneticist Richard Cawthon and colleagues at the University of Utah found shorter telomeres are associated with shorter lives. Among people older than 60, those with shorter telomeres were three times more likely to die from heart disease and eight times more likely to die from infectious disease.
If telomerase makes cancer cells immortal, could it prevent normal cells from aging? Could we extend lifespan by preserving or restoring the length of telomeres with telomerase? If so, would that increase our risk of getting cancer?
Scientists are not yet sure. But they have been able to use telomerase in the lab to keep human cells dividing far beyond their normal limit, and the cells do not become cancerous.
If we used telomerase to "immortalize" human cells, we may be able to mass produce cells for transplantation, including insulin-producing cells to cure diabetes, muscle cells for treating muscular dystrophy, cartilage cells for certain kinds of arthritis, and skin cells for healing severe burns and wounds. An unlimited supply of normal human cells grown in the laboratory would also help efforts to test new drugs and gene therapies.
Cawthon's study found that when people are divided into two groups based on telomere length, the half with longer telomeres lives an average of five years longer than those with shorter telomeres. This study suggests that lifespan could be increased five years (or more) by increasing the length of telomeres in people with shorter ones.
People with longer telomeres still experience telomere shortening as they age. How many years might be added to our lifespan by completely stopping telomere shortening? Cawthon believes 10 years and perhaps 30 years.
After age 60, the risk of death doubles every 8 years. So a 68-year-old has twice the chance of dying within a year compared with a 60-year-old. Cawthon's study found that differences in telomere length accounted for only 4% of that difference. And while intuition tells us older people have a higher risk of death, only 6% is due purely to chronological age. When telomere length, chronological age, and gender are combined (women live longer than men), those factors account for 37% of the variation in the risk of dying over age 60. So what causes the other 63%?
As discussed in the next chapter, a major cause of aging is "oxidative stress." It is the damage to DNA, proteins, and lipids (fats) caused by oxidants, which are highly reactive substances containing oxygen. These oxidants are produced normally when we breathe, and also result from inflammation, infection, and consumption of alcohol and cigarettes. In one study, scientists exposed worms to two substances that neutralize oxidants, and the worms' lifespan increased an average 44%.
Another factor in aging is "glycation." It happens when glucose, the main sugar we use as energy, binds to some of our DNA, proteins, and lipids, leaving them unable to do their jobs. The problem becomes worse as we get older, causing body tissues to malfunction, resulting in disease and death. Glycation may explain why studies in laboratory animals indicate that restricting calorie intake extends lifespan. Their extended life is likely to be a result of eating less sugary foods rather than overall calorie restriction.
It is likely that oxidative stress, glycation, telomere shortening, and chronological age (along with various genes) all work together to cause aging.
What are the prospects for human immortality?
Human lifespan has increased considerably since the 1600s, when the average lifespan was 30 years. By 2012, the average US life expectancy was nearly 79. Reasons for the increase include sewers and other sanitation measures, antibiotics, clean water, refrigeration, vaccines and other medical efforts to prevent children and babies from dying, improved diets, and better health care. Life expectancy varies considerably in different parts of the world.
Some scientists predict that average life expectancy will continue to increase, although many doubt the average will ever be much higher than about 90. But a few say vastly longer lifespans are possible. Geneticist Richard Cawthon says that if all processes of aging could be eliminated and oxidative stress damage could be repaired, "one estimate is people could live 1,000 years."
Although we cannot slow down the degradation of our telomeres as a result of aging (the passage of time), there are two very effective things we can do straight away to preserve our telomeres. As already touched upon, we can reduce oxidative stress and we can reduce glycation in our body. These are the two biggest things we can do to extend longevity and remain healthy, as explained in the next two chapters.
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Takeaway message: preserving the finite telomere capacity of the body is the key to staying healthy and living longer. This is not beyond our control. We do it by minimizing oxidative stress and glycation.
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