Understanding Cholesterol and Fat to Achieve Optimum Health

By: Michael Lam, MD, MPH


Understanding Cholesterol and Fat

Understanding cholesterol: The good and the bad.Understanding cholesterol may save your life. After decades of research, it is clear that fat and cholesterol relate to heart disease in a complex way that we have yet to fully understand. What is known is that there are good and bad fats, as there are good and bad cholesterol. The good fat and cholesterol are key macronutrients needed every day for optimum anti-aging health. Both, in their natural states, are antioxidants and protect us from free radical attacks. Understanding cholesterol and fat is complex because they can also turn bad, mostly due to commercial processing, and do harm to the body.

When understanding cholesterol one needs to know that fats and cholesterol are found intermingled in food. While fats are visible in some foods, such as bacon and French fries, it is not so noticeable in others. In contrast to fats, when understanding cholesterol, which is derived from animal products, there is no telltale signs at all. A food can be of rich in both fat and cholesterol (fried egg) or low in both (fruit and vegetables). It could also be either rich in fat but low in cholesterol (peanut butter) or low in fat and high in cholesterol (shrimp).

The secret to anti-aging lies in knowing which type is good to take, and which type is the bad type to avoid.

Fat Facts

Annual consumption of added fats such as butter, shortenings, and oils in our diet from commercially prepared cookies and fried foods now stands at 66 pounds per person per year.

Fat is one of three main macronutrient groups that supply calories in food (the other two are protein and carbohydrate). Fats in our diet come in the form of solid like the white part on a strip of bacon or as a liquid such as a vegetable oil.

Consuming some fat is essential to part of our general diet. Fats aid absorption by carrying fat-soluble vitamins A, D, E and K into the cells. Fats can add flavor to food, making them taste better in cooking. Metabolically, fat does not increase blood sugar level in our body as fast as carbohydrates.

Fat is also a superior source of concentrated energy, providing more than twice as many calories per gram as sugar, starch, or protein. While carbohydrates and protein merely provide 4 calories per gram, fat is more calorically dense with 9 calories per gram. A teaspoon of fat supplies approximately 45 calories. It doesn’t take too much fatty food to generate many calories.

The body stores energy in various forms. Excess calories consumed are converted into glycogen for storage. Glycogen storage, however, requires water to be effective. One pound of glycogen is accompanied by four pounds of water. When you go on a diet, the first source of energy the body uses is glycogen. Water is concurrently lost during this usage. This explains why crash calorie restricted diets are diuretic in nature. The initial weight lost is mostly water and not fat. This process reverses with water retention when regular diet is resumed and body weight is quickly regained. This accounts for the so call “yo-yo” weight loss syndrome, and the dieter gets discouraged.

Understanding cholesterol and muscle tissueAfter glycogen is depleted as a fuel, the body uses protein as a source of energy. The most abundant source of protein is muscle. But again, muscle tissue is 72% water by weight. A little loss of muscle protein causes a large loss of total weight.

Fat is the last storage place of energy. Since it has a unique chemical structure, fat can be stored much more competently, entailing the least amount of water to support it. Fat is stored in the adipose tissue, with about 85% of the total weight in actual fat.

Fat Chemistry

In understanding cholesterol, we must understand fat.  Fat includes what we commonly call “fats” and “oils”. “Fats” in the everyday sense are solid at room temperature while oils are liquid. Fats are made up of fatty acids that give fats their different flavors, textures, and melting points. There are two types, saturated and unsaturated. Nutritionists call both saturated and unsaturated fats “triglycerides”. A triglyceride has three fatty acids attached to a substance called glycerol.

Fat’s basic component is therefore the triglyceride, which consists of a glycerol base with three fatty acid chains attached. The difference between the various types of fats depends upon which fatty acids are in the triglyceride.

Unsaturated fatty acids (linoleic and linolenic acid) must be taken in the diet and are thus called essential fatty acids. Cholesterol is not an acid, but a type of fat found mainly in animal products such as egg yolk.

When digested, triglycerides are broken down into fatty acids and glycerol, which can then be absorbed.

Types of Dietary Fat

There are four main types of fat, each with different chemistry:

  1. Saturated
  2. Monounsaturated
  3. Polyunsaturated
  4. Trans Fat

Fats are made up of fatty acids. The main difference among fats is the extent of saturation of the chemical bonds in the fatty acids. Saturation is measured by the amount of hydrogen atoms that are connected to the carbon chain.

Saturated Fat (SFA)

Saturated fat has a fat molecular structure condensed with hydrogen, where all the existing space in the fat molecular structure is occupied. SFA contains fatty acids like stearic acid, palmitic acid, and butyric acid. Having high melting points, saturated fats are usually in solid forms at room temperature. SFA is found most in animal foods like meat, poultry, butter (which contain 66% SFA), and whole milk. Other sources of SFA include coconut, palm, and palm kernel oils. This type of fat is very visible in beef, while less visible in others such as palm oil.

In working toward understanding cholesterol, it is important to recognize that in the modern day diet, most of the SFA in our body is derived from consumption of animals reared in commercial animal farms. Not only are these animals fed hormones to speed their growth and antibiotics to prevent diseases, they are also grain fed to enhance their productivity and taste. Upon maturity, they are sent to the slaughtering house. Researches have shown that the amount of saturated fat found in such animals to be higher than those animals that are allowed to run free and fed organic food. This higher level of SFA is transferred to us upon consumption of their meat.

Understanding cholesterol from vegetable shorteningAccording to the National Health and Nutrition Examination Survey (NHANES III), the American diet contains between 14 to 18 percent saturated fat. Specific foods which contain a significant amount of saturated fat include chicken fat (30 percent), vegetable shortening (31 percent), lard (40 percent), beef fat (50 percent), butter (62 percent), palm kernel oil (81 percent), and coconut oil (86 percent).

SF also comes from hardened or hydrogenated vegetable oils (e.g. vegetable fat and hardened or hydrogenated marine/fish oils), biscuits, cakes, tarts, pie crust, pastries, chocolate, coffee creamers, milk or dairy solids, ice cream, non-dairy cream substitutes, and shortening.

While working toward understanding cholesterol, many studies have linked a high intake of SFA to increased risk of cardiovascular disease, the exact mechanism is not fully understood. It appears that the effect of SFA intake on cardiovascular disease incidence is only mediated through its effect on raising LDL cholesterol levels. If LDL cholesterol level is under control, then SFA has no independent effect. In other words, if the LDL cholesterol and HDL cholesterol levels are within normal limits, then adjustment of saturated fat intake in the diet will have little benefit.

SFA can be obtained from animal and plant sources, although animal sources are most common. The best animal source of SFA comes from cattle, poultry, and fish. Meat from free roaming grass fed cattle, poultry fed organic food instead of grain fed, or fish have the least SFA, while commercially raised grain fed cattle or chicken raised in a chicken farm have the most SFA. It’s best to obtain your SFA from consuming meat from free range animal or from vegetarian sources such as seeds and nuts. If this is not possible, consider reducing the amount of SFA by eliminating all noticeable solid fat and draining off all fat from cooked meats before consumption. A simple way is to remove the solidified fat found on top of stews a day in advance before reheating or making chili, stew, or soups. Broiling is more favorable than pan-fry meats, like hamburgers, chops, and steaks. Lean meats or extra lean meats are also recommended.

Monounsaturated Fat (MUFA)

Monounsaturated fat (MUFA) is fat that has one double bond in its structure. At room temperature, MUFA is in an oil and liquid form. When placed in the refrigerator, MUFA will turn cloudy. MUFA is derived from plant sources, such as canola (62% MUFA), peanut (49% MUFA) and olive (77%). Olive oil has the highest content of MUFA among most vegetable oils. MUFA is also found in olive oil margarine, canola margarine, and peanut butter.

MUFA is labeled as a “good” fat and for good reasons. Studies have shown that for each 10-gram increment intake of monounsaturated fat in the diet, there is a significant reduction in the relative risk for invasive breast cancer. One study published in the New England Journal of Medicine (1197; 278:2145-2150) found that stroke risk declined 11 percent for every 1 percent increase in MUFA intake in our diet.

Understanding cholesterol and fats: Olive oil is a good source of FatEpidemiological studies have shown that people that live in Mediterranean countries have one of the lowest rates of cardiovascular disease in the world. This population group takes in olive oil as their main source of fat. Olive oil is high in MUFA. Whether longevity is directly related to the high olive oil in the diet remains unknown. It has been postulated so, although there are opposing and conflicting scientific evidence, including one study where mice and monkeys fed monounsaturated fats – such as olive oil – developed more hardening of the arteries in major blood vessels than animals fed polyunsaturated fats.

MUFA’s anti-aging properties include:

  1. Lowering the oxidation of LDL cholesterol and thus, slowing a crucial process of atherosclerotic plaque formation.
  2. Lowering the triglyceride levels, a form of circulating fat found in plaque and cholesterol.
  3. Promoting high level of HDL cholesterol and hence, decreasing the risk of heart disease.

The largest benefit in terms of reduced risk of cardiovascular disease is found when SFA are replaced with MUFA. Since SFA increase risk of heart disease, and MUFA reduce that risk, changing both at the same time maximizes the benefits.

The following suggestions are recommended ways to boost MUFA in an anti-aging diet:

  1. Substitute butter with a spread that includes olive oil, which is high in MUFA.
  2. Have hazelnuts for a snack (high in MUFA) as an alternative to cheese (high in SFA).
  3. Have tossed salad with vinaigrette made from canola oil (high in MUFA), rather than ranch or Thousand Island dressing (high in SFA).
  4. Cook exclusively with olive (high in MUFA). Olive oil is the best of all oils for consumption. Use the extra virgin form in a glass that is opaque and store it away from light to avoid oxidation of the fats in the oil.

Polyunsaturated Fat (PUFA)

Polyunsaturated fat (PUFA) are fat made up with fatty acid chains (like linoleic acid and linolenic acid) that contains two or more double bonds. PUFA are primarily found in vegetable oils and fish sources. Omega-6 PUFA is derived from vegetable oils. Salad dressing, margarine, and mayonnaise containing these oils are therefore high in PUFA. Omega-3 PUFA are found primarily in fish. At room temperature, PUFA is in liquid form. Even in cold temperatures, PUFA still remains as liquid since it has a lower melting point than MUFA or SFA.

Cooking oils (which are natural mixtures of various fatty acids) are mostly a mixture of MUFA and or PUFA. Olive oil is a good example of mostly monounsaturated fatty acids (77% MUFA), while canola oil has 32% PUFA. Most common vegetable oil such as soy (61% PUFA), safflower (77% PUFA), and sunflower (69% PUFA) oil, are high in polyunsaturated fats.

Understanding cholesterol and PUFA cooking oilsThe push towards PUFA vegetable oil worldwide from the early 1970s have lead to a tremendous increase in PUFA in our body. Research studies revealed that natural virgin PUFA lowers cardiovascular disease risk by 19% in some studies. Unfortunately, most PUFA consumed these days, like corn, soy, or safflower are often commercially processed. Their molecular structure is greatly modified. The health enhancement properties of PUFA have largely been lost in this process.

Original healthy sources of natural PUFA are found in nuts and seeds. Also, cold water fish such as salmon contain a good amount of PUFA. The PUFA found in processed vegetable oil such as corn oil is structurally changed and not good for the body.

Trans Fat

Both MUFA and PUFA tend to be liquid at room temperature. In order to firm them up, food processors will ” hydrogenate” PUFA. This processing results in a type of fat call trans fat. Trans fat remains solid at room temperature. They can be then turned into shortening and margarine. By increasing its resistance to oxidative damage, the oil’s shelf life is extended. Its commercial value is increased. Trans fat is commonly used in cakes, donuts, fast foods, and fried foods. It is estimated that Americans consume about 5 grams of trans fat per day, accounting for about 3 percent of their total calories, according to at 1999 study reported in the Journal of the American Dietetic Association.

While trans fatty acids may be classified as hydrogenated polyunsaturated fats due to their chemical structure, they generally are like saturated fats in terms of their effects on cholesterol.

Without a doubt, trans fat is the worse kind of fat. During the hydrogenation process, the chemical structure of the natural fatty acid is changed from their original cis- configuration to unnatural trans- configuration. Trans-isomerization alters the 3 dimensional configuration of dietary fatty acid, causing damage to the cell membranes and altering the function of phospholipid-dependent enzymes contained in these membranes. This altered fluidity increase cell membrane permeability. The active transport enzymes for sodium, potassium, calcium, and magnesium are impaired. Such cell membrane is also subject to free radical attack and damage. A high intake of trans fat has therefore been linked to a variety of free radical and degenerative conditions such as cancer, arthritis, and cardiovascular disease.

Trans fat also increases the level of triglyceride and LDL cholesterol. More significantly, trans fat reduces the level of “good” HDL cholesterol that often related to the lower risk of cardiovascular diseases. A study published in the New England Journal of Medicine reported that trans fat is linked to a 93% rise in the risk of cardiovascular disease. The research also revealed that a replacement of 2% of trans fat consumed with MUFA (like nuts, olive oil and flaxseed oil) could reduce heart disease risk by 53%.

Understanding cholesterol and how trans fats affects your bodyTrans fats should be avoided as much as possible in our diet. Trans fats are exposed to heat and oxygen during the frying process results in the worse possible combination of unhealthy fatty acids. Also, salad oils used in producing salad dressing like mayonnaise also have excessive amount of lipid peroxides. Studies have shown that the average woman age 19-50 got more fat from salad dressing than from any other food!

Naturally occurring trans fat is quite rare, being limiting to a small amount in milk as a consequence of gut bacteria in dairy cows. Clearly this is not the kind of fat Mother Nature intended us to have in our body.

Consumers as a whole are quite ignorant of the negative effect of trans fat. Look for the term “partially hydrogenated” to disclose its presence on food labels. Those who try to assess the amount of trans fat in the food will find it difficult, because the Food and Drug Administration (FDA) does not require manufacturers to specify the amount of trans fat on the food label. Margarine, for example, may provide 3 grams of saturated fat per tablespoon. They are, however, very high in trans fat, with as much as 3 additional grams per tablespoon. Chocolate chips cookies that contain only 2 grams of saturated fat according to the label may contain double that amount of trans fat, though this is not seen on the label. Anytime you see the word “hydrogenated fat” on the label, you are looking at trans fat. The easiest way to calculate is to look at the total fat at the label and subtract the amount of monounsaturated, polyunsaturated, and saturated fat.

Fat and Cholesterol in Food

Approximate amount of fat and cholesterol in Food
Food Category Serving size Grams fat per serving Cholesterol (mg/dl)
Dairy
Ice cream 1 cup 15 60
Egg, cooked 1 5 210
Cheddar cheese 1 oz. 10 30
Meat
Regular ground beef cooked 1 patty 15 90
Hot dogs 1 15 35
Chicken leg w/skin 1 15 105
Nuts and seeds
Peanut butter 1 Tbsp. 10
Baked goods
Doughnut, glazed 1 10 10
Brownies 1 square 5 15
Candy
chocolate 1 oz. 10 10
Other
olives, giant size 5 5
* 1 gram of fat or cholesterol has 9 calories

Fatty Acids (FA)

Fat is made up of fatty acids and play a role in understanding cholesterol. Fatty acids are chains of carbon atoms (usually 16-20 carbon atoms long) which can either be saturated with hydrogen atoms (the saturated fatty acids normally found in animal fats) or contain relatively fewer hydrogen atoms (the unsaturated and polyunsaturated fatty acids commonly found in vegetable fats and oils). At one end of the chain is an acid group. Although this fatty acid configuration may seem straightforward, prospective changes in its structure can lead to a huge difference set of entities that perform quite varying roles in the body. It is therefore more accurate to describe fats as those which contain fatty acids, and it is the fatty acids that can be saturated, monounsaturated, or polyunsaturated.

Understanding cholesterol and fatty acids as building blocksWhen understanding cholesterol, it is important to recognize that fatty acids are essential building blocks for vital functions in the body. They perform a variety of specific and essential functions. First, fatty acids form an integral component of the plasma membrane of every cell in the body. This membrane is the shell around a cell and protects the cell. The membrane of a cell is a very active location because signals from outside the cell are directed to the cell at its surface where numerous receptors and transport pumps are situated. The composition of the cell membrane in terms of the fatty acids that make up the membrane are known to affect the quality and degree of signaling across the membrane. This function is crucial since cellular responses to hormones, uptake of nutrients, and discharge of waste all require activity at the membrane. Vital transport pumps located at the cell membrane include the sodium/potassium and calcium/magnesium pump. Unhealthy cell membrane leads to a pump breakdown, cellular dysfunction, and eventual cell death.

Essential Fatty Acids (EFAs)

Our bodies cannot make all fats we need. There is a subset of dietary fatty acids known as essential fatty acids (EFAs) which are essential for normal body function but that cannot be made endogenously and must be consumed.

EFAs are vital for a healthy immune system. EFAs also assist the body in disintegrating SFA and helping the body to get rid of it. Moreover, EFAs also adjust cholesterol metabolism rate.

The two most important group of EFA is called omega-6 (N6 EFA) omega-3 (N3 EFA). Both come from consumption of PUFA and MUFA.

Omega-6 (N6) EFA is found in safflower, sunflower, corn, and evening primrose oils. There are many subgroups within this family of EFA. The primary head of the N6 EFAs family is Linoleic acid. Other sub-divisions to this similar category are GLA and ARA.

Omega 3 (N3) EFA is derived from olive, flaxseeds, walnuts, soybeans, and freshly ground wheat germ. These are sold in most health food stores. The chief of the N3 EFA family is Linolenic acid (ALA).

These two groups are also not inter-convertible with each other once inside our body.

EFAs Deficiency

Unfortunately, more than 50 percent of the population is not getting enough N3 EFAs and may have a N3 EFA defficiency. N3 EFA is critical for eye, brain, and neurological function. Deficiencies of N3 EFAs can cause impaired brain function and decreased IQ. N3 EFAs is also a blood thinner that prevents platelet aggregation and strokes. Too much of anything is generally not good. Excessive N3 EFAs worsen diabetes and bleeding.

N6 EFA is also important in understanding cholesterol. It plays a major role in the texture and appearance of the skin and blood vessel structure. N6 EFA deficiency has a negative effect on the circulatory system. Understanding cholesterol and flax as a source of EFAsSymptoms include increased triglyceride, cholesterol, and blood pressure; hardening and obstruction of arteries; abnormal hair loss; increased urination; and skin disorders.

EFAs can be found in many vegetables such as soybean, flax, walnuts, and green leafy vegetables. The average adult requires 0.3 gram per kg ideal body weight per day. This translates into 20 grams for the average 70 kg adult. Fish is a good source of N3 EFAs. Poultry, eggs, and lean meat contain both N6 and N3 sub-fractions such as GLA, ARA, EPA, and DHA.

Certain fish in particular are very rich in EFAs. Sardines (about 3.3 grams of N3 EFA in three ounces) and mackerel (2.5 grams per 3 ounces) are good examples. For non-fish eaters, marine plants like seaweed also supply N3s, and health food stores carry oil supplements rich in N3. Many are not used to taking fish oil, which in high amounts, can cause a fishy “burp”. Because they’re highly unsaturated (more so even than other polyunsaturated fats), N3s are very susceptible to oxidation and turn rancid rapidly, a metamorphosis that undermines their value to cell membranes. For that reason, fish oil supplementation should be accompanied by fat-soluble antioxidant vitamin E. Store your oils in the fridge as well as in opaque bottles will also slow down the oxidative process.

Consuming an adequate amount of fish (8 to 10 ounces a week) is the easiest way to prevent any EFA deficiencies.

N6 to N3 EFA Balance

The amount of N6 EFA and N3 EFA in food depends on the kind of PUFA taken in and varies greatly depending from food to food. It is now known that the ratio of N6 to N3 EFA is a more important indicator of optimum health than the absolute amount of PUFA intake. This is similar to cholesterol, where the ratio of HDL cholesterol and LDL cholesterol to total serum cholesterol is more important than the serum cholesterol level itself as predictor of cardiovascular heath.

The ratio of N6 to N3 EFA is crucial for anti-aging. The traditional hunting diet of our ancestors consisting of lean meat, vegetables, fruits, nuts and seeds maintained a N6 to N3 ratio of 4:1. The optimal N6 to N3 EFA ratio should be close to this according to many in anti-aging research. The modern day processed food diet using processed PUFA and trans fat has far more N6 than N3 EPA. The dietary problem stems not just from the vegetable oils we eat, which are rich in N6, but also in today’s commercially raised and prepared eggs and meat, which contain a lower percentage of N3 than they once did. Consequently our diets contain a lopsided ratio of N6 to N3 that is estimated to be 20 or more to 1. It may be interesting to note that organic free-range eggs (eggs from chicken fed organic food and run free) have a N6 to N3 EFA ratio of close to 1 to 1, while eggs from commercial chicken farms have a N6 to N3 EFA ratio of 19 to1. Many studies have linked low levels of N3 fatty acids in the blood with depression, attention deficit disorder, and cardiovascular diseases.

Understanding cholesterol, fats, and fishHaving a rich amount of N3 EFA as part of the PUFA, cold-water fish like salmon may be considered one of the finest foods in an anti-aging diet. In the famous Diet and Reinfarction Trial (also known as the DART trial), it was shown that 300 grams (10 ounces) of fatty fish every week (comparable to 2-3 grams of EPA, the breakdown product of N3) could lower post myocardial infarction mortality by 29% when compared to controls. In fact, the control group was on a standard fat reduction diet, which on the average had lower cholesterol levels than the subject group.

Fat and Cardiovascular Disease

The hypothesis that consuming a great amount of fat in diet will lead to cardiovascular disease is outdated and needs further understanding. While some fats are essential for good health, like MUFA and PUFA, other such as trans fat is harmful to our bodies. Therefore, it is the type of dietary fat that matters and not the total amount of fat consumed that decides the cardiovascular disease risk.

This has been well documented in population studies. For example, Greeks consume much lesser SFA and more MUFA (in olive oil) as compared to the Americans, even though they may have similar fat intakes. They also have one of the lowest rates of heart attacks in the world. Japanese who live in Japan have the lowest rate of heart attacks in the world. They also consume an abundance of raw fish (sashimi) that are high in natural SFA and N3 EFA (from the PUFA in the meat of the fish). The lower rates of cardiovascular disease is not directly related to total fat intake, but more with the kind of fat consumed. This is further confirmed by studies within Japan, where it is found that the incidence of cardiovascular disease among fishing villages is lower than farming villages, where the diet is higher in grain.

“Traditional medical wisdom since the 1970s encourages a reduction of fat intake as a way to reduce cholesterol level. Americans are consuming more than 40% of its calories in fat; this should be reduced to 30% and not lower. While some people restrict fat to 20%, there are other enthusiasts that even considered reducing fat intake to 10% or less of caloric intake. Extreme low fat intake level is difficult to achieve without foregoing food and appetizing choices. A diet extremely low in fat has been linked to an increase in cancer and strokes, primarily through the free radical pathology pathway. It should be noted up to 30% of the adult population should not be on a low-fa , high carbohydrate diet. Instead, they should be on a high-fat (45%, comprising mostly of monounsaturaed and polyunsatuated fat), low protein (15%), and moderate complex carohydrate (40%) dietbecause they suffer from insulin resistance (or Syndrome X). This condition is caused by over-consumption of carbohydrates over a long period of time, and it is linked to a high risk of cardiovascular disease.”

Understanding cholesterol and carbs as a risk factorAny focus on a single dietary discipline should be taken with care. In understanding cholesterol, the proper choice of fat in the diet is more important than the absolute amount. The general delusion that low fat diet causes low cardiovascular risk without considering the kind of fat taken in must be dismissed. Sad to say, most people replace fat with protein and carbohydrates when they reduce their fat intake. Carbohydrate such as pasta, rice, cereal, and potato are chosen. This is actually worse as a high carbohydrate diet increases insulin, reduces HDL cholesterol, and increases triglycerides. In understanding cholesterol, knowing the details on what to eat is critical. The popular notion of a high carbohydrate diet of the last 30 years has produced an obese population never seen before in human history and an epidemic of adult onset diabetes.

Fat Recommendation

A well-balanced proportion of fat is the key to healthy aging. When understanding cholesterol, it is important to recognize that a diet too low in fat may actually bring harm to health. The correct way is to discern the right type to take and those to avoid. The overall fat intake as a percentage of dietary calories should not fall below 30%. To have plenty of “good” MUFA like olive oil, seeds, nuts, and cold-water fish that have high N3 content. Saturated fat is necessary for good health. It could come from animal or plant sources. To express your understanding cholesterol choose free-range poultry or beef, organic eggs, and deep-water fatty fish such as salmon. It is very important to avoid “bad” trans fat, like margarine and fried foods. Moreover, the use of processed PUFA such as corn, safflower or sunflower oil should be restricted.

Out of the 30 % recommended daily calorie from fat sources, less than one third should be saturated fat, the rest should come from mono-unsaturated fat as much as possible.

Here are some practical tips:

  • Trim visible fat from all cuts of meat.
  • Include one to two fish or seafood meals a week (total 8 ounces). Open water cold-water oily fish such as salmon or tuna is preferred.
  • Don’t batter or fry fish in animal or hydrogenated vegetable fats; pan-frying and deep-frying may decrease the omega-3 content of the fish.
  • Switch to low fat or non-fat varieties of milk and other dairy products.
  • Instead of frying foods, try steaming, stir-frying, or baking.
  • Limit take-out foods, butter, potato chips, biscuits and cake, and other processed food containing vegetable shortening (trans fat).
  • Choose fat from unrefined sources – for example, oily fish, nuts, soy, avocado, seeds (in bread), and virgin/cold pressed oils.
  • Use a virgin olive oil, if available.
  • Use non-stick cooking pans to cut back on the amount of fats that are used solely to stop the food from sticking.

Cholesterol

When attempting to control cholesterol one must know, exactly what it is, because understanding cholesterol brings you closer to balancing it. A waxy substance consisting of fats (lipids) and proteins, cholesterol is a necessity for life. Cholesterol is carried around in the blood on carrier molecules called lipoproteins. The main lipoproteins categories are namely very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density-lipoprotein (HDL). Once bound to the carrier HDL, the cholesterol is known as HDL cholesterol. HDL in effect transports fat from the cell to the liver. When the HDL cholesterol level is high, it is more cardio protective. Therefore, HDL cholesterol is considered “good ” cholesterol. LDL is the carrier of oxidized cholesterol as LDL cholesterol from the liver to cell. Elevated LDL cholesterol is directly correlated with increased cardiovascular risk. LDL cholesterol is therefore called the “bad” cholesterol.

Understanding cholesterol and how it guards the cell membranesIn understanding cholesterol, it is important to note that cholesterol, when unoxidized, is an antioxidant and free radical scavenger in its naturally occurring state. In fact, cholesterol guards the cell membranes’ phospholipid from free radical damage and protects it against atherosclerosis, cancer, and other free radical attack. Also, cholesterol is a predecessor to many steroid hormones and vitamin D. Cholesterol is produced at the liver at the rate of 3,000 to 4,000 mg daily in the liver.

When truly understanding cholesterol, the notion that total blood cholesterol level alone is the key determinant of cardiovascular heath should be dispelled. Polar bears, for example, maintain a total blood cholesterol of over 400 mg/dl and they seldom develop heart attacks. There is obviously a lot more to learn about cholesterol and its link to cardiovascular disease that we currently know.

Understanding Cholesterol and Free Radical Activity

While the exact mechanism of how cholesterol affects our body is still under intense investigation, it is clear that our understanding cholesterol leads us to a unified theory of free radical damage caused by unhealthy foods such as processed fat and cholesterol is the most likely mechanism. Free Radical damage to our blood vessels is one of the primary causes of atherosclerosis. The most important cause of free radical pathology is the excessive dietary fat consisting of processed PUFA trans fat frequently used in fried foods, margarine, and cooking oil, and oxidized cholesterol from commercially prepared foods. In the event that dietary fat and oil is retrieved from fresh, whole, and unprocessed foods, no lipid peroxidation will take place and the cell membrane will remain healthy in a normal cis-configuration without any free radical damage.  This information is essential to understanding cholesterol and how to manage it.

One theory advanced by the late Nobel laureate Dr. Linus Pauling, together with his research cohort Dr. Matthias Rath, knowledgable scientists in understanding cholesterol, is that the total serum cholesterol is really an indicator of the amount of free radical damage in the body. Our body maintains an optimum level of total cholesterol level as well as a delicate balance among its sub-components. A negative feedback mechanism exists within the body that decreases the rate of endogenous synthesis when the dietary intake is exceeds what is needed. The total circulating cholesterol therefore remains relatively constant at between 170-200 mg/dl for the normal adult. The higher the free radical level, the higher the body needs to produce cholesterol internally from the liver to act as an antioxidant and free radical scavenger. In fact, a low total cholesterol level (below 150 mg/dl) has been linked with an increased risk of cancer and stroke.  This is critical knowledge in properly understanding cholesterol.

It is important in understanding cholesterol that cholesterol in its natural state is therefore actually good for us. During commercialization, lipid (including fat and cholesterol) peroxidation takes place as soon as fats and oils are extracted from the foods in which they naturally occur. This commercialization process is speeded up by metallic ions, particularly iron and copper. Extensive lipid peroxidation can occur without an apparent stale or flavor, like in peanut butter, the making of salad and cooking oil, and also in so-called cold-pressed oils. During the processing of PUFAs to make cooking oil, rapid peroxidation can take place and free radicals are released. This process is accelerated by heat, atmospheric oxygen, light, and trace amounts of unbound metallic elements.

Understanding cholesterol and peroxidationOxidized cholesterol is a free radical generator and an important factor in understanding cholesterol. It is attached particularly to low-density lipoproteins as LDL cholesterol as it goes from the liver to the cell. Hamburgers and other cooked and processed foods contain animal fats that are usually high in oxidized cholesterol when cooked. Foods cooked in animal fat and fried in processed PUFA (such as corn oil) also have high oxidized-cholesterol content. As a result, the higher the LDL cholesterol level, the higher the risk of cardiovascular disease. In an effort to understanding cholesterol better scientists have studied rabbits. Research has shown that rabbits that consumed a small amount of oxidized cholesterol for merely 12 weeks had atherosclerosis plaques that were two times as big as the control population. Studies reveal that heart attack risk falls 2% for every 1% drop in LDL cholesterol level. This information helps in our understanding of cholesterol.

One of the most important causes of free radical pathology is the excessive dietary fat consisting of processed PUFA or trans fat frequently used in fried foods, margarine, and cooking oil. In the event that dietary fat and oil is retrieved from fresh, whole, and unprocessed food, no peroxidation will take place and cell membrane will remain healthy in a normal cis-configuration without any free radical damage. Studies have shown that 20% of dietary calories as commercially available fat will not surpass the control threshold of endogenous free radical protection. Unfortunately, the current contribution from such fat to our diet exceeds 40 percent which is critical knowledge in understanding colesterol.

Lipoprotein(a)

When understanding cholesterol it is important to realize that some of the natural cholesterol produced by the liver in response to free radical damage is converted into LDL cholesterol and its relative lipoprotein(a) (Lp(a)). While LDL cholesterol maybe known as the “bad” cholesterol, Lp(a) is even worse. Lp(a) is a plasma lipoprotein that structurally resembles LDL, but with an additional adhesive protein. Lp(a) is also made in the liver and transported to the cell. Studies have shown that Lp(a) holds fast to damaged blood vessel, attracting other Lp(a) molecules, and finally constituting the athrosclerotic plaques. In fact, a high Lp(a) level (more than 30 mg/dl) has been revealed to carry a 10 times greater risks for heart disease that LDL cholesterol level. Lp(a) level should be part of a routine blood screening test for cardiovascular disease risk.

Lp(a), according to Drs. Pauling and Rath, is the body’s way of repairing its damaged vessel wall that has micro leakages caused at least in part by free radical damage and vitamin deficiencies (more specifically vitamin C ). Humans do not make any endogenous vitamin C and have no self-repair mechanism of the vascular system. Lp(a) is used by the body as a surrogate vitamin C, so to say. Lp(a), unfortunately, has a sticky characteristic and adheres to each other, forming an atherosclerotic plaque over time. The body, at the interim, is unaware. As long as the damage persists due to free radical presence (either from improper diet, aging, pollution, lack of vitamins, or toxins), the body responds by making more cholesterol endogenously in the liver, feeding a viscous cycle of ever increasing Lp(a). This knowledge is important in understanding cholesterol.

Understanding Cholesterol and Cardiovascular Disease

Understanding cholesterol and coronary heart disease risksFor those with knowledge, understanding cholesterol doesn’t means lowering cholesterol reduces coronary heart disease risks. To make matters worse, such “low-fat, high carbohydrate” diets are often high in the wrong type of carbohydrate. Instead of taking in complex, paleo type carbohydrates such as green leafy vegetables, the ignorant consumer often ends up eating foods such as pasta, soda, processed foods, and fast foods. These types of food are rich in sugar and starch (carbohydrate). They actually lower the important “good” HDL cholesterol. When understanding cholesterol one must recognize that an HDL cholesterol level is inversely proportional to the cardiovascular disease risk. It should be remembered that cholesterol and fat are concentrated sources of calories and can lead to obesity if consumed too much.

In the Framingham study for example, men and women consumed an average cholesterol intake of 700 mg and 500 mg per day respectively were studied (one egg provides 200 mg). The average serum concentration of cholesterol for men and women with higher than average cholesterol intake were found to be 237 and 245 mg/dl respectively. Subjects with lower than average intakes were found to be 237 and 241 mg/dl. The difference is statistically insignificant. Statistically, studies have showed that people who consume 4 eggs per week (one egg provides 200mg cholesterol) actually have average serum cholesterol (193 mg/dl) same than those who reported consuming only 1 egg per week (197 mg/dl). Clearly dietary cholesterol in and of itself is not the critical link to heart disease risks as we once thought.

How Much Cholesterol Should You Consume?

A low total serum cholesterol level is undesirable for the healthy person. It is very difficult to lower cholesterol only without other types of fats because they are often found intermingled with each other in food. While SFA from animal and diary products is not subject to lipid peroxidation, all animal fats contain some PUFA and cholesterol, both of which undergo auto-oxidation. Those who are serious about understanding cholesterol and reducing total serum cholesterol level should refrain from intake of lipid peroxide-containing fats (trans fat such as margarine) with resulting reduction of free radical pathology. Like trans fat, oxidized cholesterol should be limited as much as possible.

Understanding cholesterol means knowing that a low fat diet may actually bring harm to health. The correct way is to discern the right type to take and those to avoid. The overall fat intake as a percentage of dietary calories should not fall below 30%. One should have plenty of “good” MUFAs like olive oil, seeds, nuts, and cold-water fish that have high N3 content. Saturated fat is necessary for good health and understanding cholesterol means it should come from free-range poultry or beef, and organic eggs. It is very important to avoid “bad” trans fat, like margarine and fried foods. Moreover, the use of processed PUFA such as corn, safflower or sunflower oil should be restricted.

Laboratory Standard

From a laboratory test perspective, the following parameters should be considered for optimum anti-aging:

  • Maintain a healthy total cholesterol level at the upper limit of normal at around 200 mg/dl.
  • High HDL level (more than 50 mg/dl) and a low LDL level (less than 130 mg/dl).
  • Total cholesterol /HDL cholesterol ratio of less then 4.
  • LDL/HDL cholesterol ratio of less then 2.5.
  • Triglyceride level of under 150 mg/dl.

Understanding cholesterol and green leafy vegetablesWhen understanding cholesterol it is important to know that the best way to accomplish is to limit the amount of simple refined carbohydrates (sugar), processed polyunsaturated fats (corn oil), and trans fats (donuts and fast foods), while maintaining a balanced diet of complex carbohydrates (green leafy vegetables), saturated fat from free range animals (as in meat and butter), and moderate amount of cholesterol (in meat and eggs).

Summary: Understanding Cholesterol

Fat and cholesterol are necessary macronutrients for optimum health. In understanding cholesterol the key lies in selecting the right source, followed by the proper preparation.

Understanding cholesterol is not as necessary for those who are vegetarians. They will not have much difficulty as fat and cholesterol in its natural state is found in abundance in seeds and nuts. Those who cannot do without meat face a more challenging task. The reason is because during the commercialization process, the chemical structure of the macronutrients within the meat is altered significantly.

Understanding cholesterol means recognizing that saturated fats possess the ability to raise both LDL and HDL levels. Polyunsaturated fats will lower both, while monounsaturated fats are relatively neutral with a small tendency to raise HDL and lower LDL. This recognition and appreciation suggests dietary approaches for influencing cholesterol levels beyond simply blind fat reduction.

It is impractical to eat only the “good ” and avoid all the “bad” fat and cholesterol, since most food comes with a combination of both. Balance is the key. Concentrate your diet on monounsaturated fats such as olive oil and saturated fats derived from free-range animals. Bad fat such as processed polyunsaturated fat or trans fat should be avoided.

Understanding cholesterol means understanding what you eat. Fat and cholesterol often are found in meats, and meats can provide many important nutrients. Many people think chicken and fish are healthier than red meat. Red meats can be low in fat and included in a healthy-heart diet, if properly selected and cooked (without frying in processed oil). Remember, chicken and fish, which often are low-fat choices, can be prepared (such as deep frying) so they are higher in fat than lean beef or pork. Dark meat poultry has more fat than white meat. Keeping the skin on chicken or frying it adds more fat. What you buy at the supermarket and how you cook the food makes the difference. If possible, always buy free-range beef and poultry.

Understanding cholesterol doesn’t mean lowering the total serum cholesterol alone, or resorting to a low fat diet should not be the goal, as it has no significant bearing on the overall cardiovascular health.

 

ReferencesAbbasi F, McLaughlin T, Lamendola C, Kim HS, Tanaka A, et al: High carbohydrate diets, triglyceride-rich lipoproteins, and coronary heart disease risk. Am J of Cardiology 85(1):45-48, 2000.

Ascherio A, et al: Health effects of trans fatty acids. American Journal of Clinical Nutrition 66:1006s-1010s, 1997.

Ascherio A, Katan MB, Stampfer MJ: Trans Fatty Acids and Coronary Heart Disease. N Engl J of Med 340(25):1994-8, 24 June 1999.

ASCN/AIN Task Force on Trans Fatty Acids: Position paper on trans fatty acids. American J of Clin Nutr 63:663-670, 1996.

Aviram M, et al: LDL oxidation by arterial wall macrophages depends on the oxidative status in the lipoprotein and in the cells: role of prooxidants vs. antioxidants. Mol Cell Biochem 188(1-2):149-59, Nov 1998.

Brown MS, Goldstein JL: Receptor-mediated control of cholesterol metabolism. Science 191:150-154, 1976.

Chen YD, Swami S, Skowronski R, Coulston AM, Reavan GM: Effect of variation in dietary fat and carbohydrate intake on postprandial lipemia in patients with non insulin dependent diabetes mellitus. J Clin Endocrinol Metab 76:347-51, 1993.

Chen YDI, et al: Effect of acute variations in dietary fat and carbohydrate intake on retinly ester content of intestinally derived lipoproteins. J Clin Endocrin Metabolism 74:28-32, 1992.

Collier GR, et al: The acute effect of fat on insulin secretion. J Clin Endocrin Metabolism 66:323-326, 1998.

Cordain L, Gotshall RW, Eaton SB: Evolutionary aspects of exercise. World Review of Nutr and Diet 81:49-60, 1997.

Cordain L, Martin C, Florant G, Watkins BA: The fatty acid composition of muscle, brain, marrow and adipose tissue in elk: evolutionary implications for human dietary lipid requirements. World Review of Nutr and Diet 83:225, 1998.

Costantini F, Pierdomenico SD, De Cesare D, De Remigis P, Bucciarelli T, et al: Effect of Thyroid Function on LDL Oxidation. Arterioscler Thromb Vasc Biol 18:732-737, 1998.

Coulston AM, et al: Plasma glucose, insulin and lipid responses to high-carbohydrate, low-fat diets in normal humans. Metabolism 32:52-56, 1983.

Crawford MA, et al: Linoleic acid and linolenic acid elongation products in muscle tissue of syncerus caffer and other ruminant species. Biochem J 115:25-27, 1969.

Denke MA, Grundy SM: Effects of fats high in stearic acid on lipid and lipoprotein concentrations in men. American J of Clin Nutr 54:1036-1040, 1991.

Despres J-P, Lamarche P, Mauriege P, et al: Hyperinsulinemia as an independent risk factor for ischemic heart disease. N Engl J Med 334:952-57, 1996.

Dietschy JM: Theoretical considerations of what regulates low-density lipoprotein and high-density lipoprotein cholesterol. American J of Clin Nutr 65:1581S-1589S, 1997.

DiPalma JR, Thayer WS: Use of niacin as a drug. Annu Rev Nutr 11:169-187, 1991.

Everson GT, Daggy BP, McKinley C, Story JA: Effects of psyllium hydrophilic mucilloid on LDL-cholesterol and bile acid synthesis in hypercholesterolemic men. J Lipid Res 33(8):1183-92, 1992.

Frost G, Leeds A, Trew G, Margara R, Dornhorst A: Insulin sensitivity in women at risk of coronary heart disease and the effect of a low glycaemic index diet. Metabolism 47:1245-51, 1998.

Gardner CD, et al: Monounsaturated versus polyunsaturated dietary fat and serum lipids. A meta analysis. Arterioscler Thromb Vasc Biol 15:1917-1927, 1995.

Gey KF, et al: Inverse correlation between plasma vitamin E and mortality from ischemic heart disease in cross-cultural epidemiology. Am J Clin Nutr 53:326S-334S, 1991.

Ginsberg HN, Kris-Etherton P, Dennis B, Elmer PJ, Ershow A, Lefevre M, et al: Effects of Reducing Dietary Saturated Fatty Acids on Plasma Lipids and Lipoproteins in Healthy Subjects: The Delta Study, Protocol 1. Arterioscler Thromb Vasc Biol 18:441-449, 1998.

Grundy SM: Comparison of monosaturated fatty acids and carbohydrates for lowering plasma cholesterol. N Engl J Med 314:745-748, 1986.

Harris WS: n3 fatty acids and serum lipoproteins: human studies. American J of Clin Nutr 65:1645s-1654s, 1997.

Hollenbeck CB, et al: Effects of sucrose on carbohydrate and lipid metabolism in NIDDM patients. Diabetes Care 12:62-66, 1989.

Howell WH, et al: Plasma lipid and lipoprotein responses to dietary fat and cholesterol: a meta-analysis. American J of Clin Nutr 65:1747-1764, 1997.

Illingworth DR, et al: Comparative effects of lovastatin and niacin in primary hypercholesterolemia. Arch Intern Med 154:1586-1595, 1994.

Jenkins DJ, Wolever TM, Taylor RH, et al: Slow release dietary carbohydrate improves second meal tolerance. Am J Clin Nutr 35:1339-46, 1982.

Jeppesen J, Facchini FS, Reaven GM: Individuals with high total cholesterol/HDL cholesterol ratios are insulin resistant. J Intern Med 243:293-98, 1998.

Jialal I, et al: The role of oxidized low density lipoprotein in atherogenesis. J Nutr 126(4 Suppl):1053S-7S Review, April 1996.

Jialal I, et al: Effect of combined supplementation with alpha-tocopherol, ascorbate and beta carotene on low-density lipoprotein oxidation. Circulation 88(6):2780-6, Dec 1993.

Kalopissis AD, et al: Inhibition of hepatic very-low-density lipoprotein secretion in obese Zucker rats adapted to a high-protein diet. Metabolism 44:19-29, 1995.

Katan MB, et al: Congruence of individual responsiveness to dietary cholesterol and to saturated fat in humans. J of Lipid Research 29:883-892, 1998.

Keys A, et al: Serum cholesterol response to changes in the diet. IV. Particular saturated fatty acids in the diet. Metabolism 14:776-787, 1965.

Krauss RM, Dreon DM: Low-density lipoprotein subclasses and response to a low-fat diet in healthy men. Amer J of Clin Nutr 62:478s-487s, 1995.

Leaf A, et al: Cardiovascular effects of n3 fatty acids. N Engl J of Med 318:549-557, 1988.

Lichtenstein AH, Ausman LM, Jalbert SM, Schaefer EJ: Effects of Different Forms of Dietary Hydrogenated Fats on Serum Lipoprotein Cholesterol Levels. N Engl J of Med 340(25):1933-40, 24 June 1999.

Liu S, Stampfer MJ, Manson JE, Hu FB, Franz M, Willett WC: A prospective study of glycaemic load and risk of myocardial infarction in women. FASEB 12:A260(abstr), 1998.

Louheranta AM, et al: Linoleic acid intake and susceptibility of very-low-density and low-density lipoproteins to oxidation in men. Amer J of Clin Nutr 63:698-703, 1996.

MacRury SM, Muir M, Hume R: Seasonal and climatic variation in cholesterol and vitamin C: effect of vitamin C supplementation. Scott Med J 37(2):49-52, 1992.

Mennen L, de Maat M, Meijer G, Zock P, Grobbee D, Kok F, Kluft C, Schouten E: Factor VIIa Response to a Fat-Rich Meal Does Not Depend on Fatty Acid Composition: A Randomized Controlled Trial. Arterioscler Thromb Vasc Biol 18:599-603, 1998.

Mensink RP, et al: Effects of monounsaturated fatty acids versus complex carbohydrates on high-density lipoproteins in healthy men and women. Lancet 1:122-125, 1987.

Mensink RP, Katan MB: Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arterioscler Thromb 12:911-919, Aug 1992.

Nelson GJ, et al: Low-fat diets do not lower plasma cholesterol levels in healthy men compared to high-fat diets with similar fatty acid composition at constant caloric intake. Lipids 30:969-976, 1995.

Oxidized Cholesterol in the Diet Accelerates the Development of Aortic Atherosclerosis in Cholesterol-Fed Rabbits. Arterioscler Thromb Vasc Biol 18:977-983, 1998.

Reaven GM: Pathophysiology of insulin resistance in human disease. Physiol Rev 75:473-486, 1995.

Schaefer EJ, Lichtenstein AH, Lamon-Fava S, et al: JM Effects of National Cholesterol Education Program Step 2 diets relatively high or relatively low in fish-derived fatty acids on plasma lipoproteins in middle-aged and elderly subjects. Am J Clin Nutr 63(2):234-41, 1996.

Siguel E: Essential fatty acid status in patients. J Parenter Enteral Nutr 1(4):243, July-Aug 1997.

Siguel E: A new relationship between total/high density lipoprotein cholesterol and polyunsaturated fatty acids. Lipids Suppl:S51-6, 31 March 1996.

Siguel E: Making sense of fats: How fatty acids regulate health and disease states. Fatty Acid Metabolism, FA Abnormalities in Gastrointestinal and Cardiovascular Disease, Fats for Dyslipidemia and Premature Coronary Artery Disease, Dietary eggs increase – 3 levels in subjects with dyslipidemia. <http://www.efafood.com/research.htm>

Siguel E, Lerman RH: The effect of low-fat diet on lipid levels. JAMA 275(10):759-60, 13 March 1996.

Siguel E, MacBeath BR, Lerman RH: Very low-fat diets for coronary heart-disease: perhaps, but which one? JAMA 275(18):1402-3, 8 May 1997.

Siguel EN: Dietary modulation of omega-3/omega-6 polyunsaturated fatty acid ratios in patients with breast cancer. J Natl Cancer Inst 90(8):629-31, 15 April 1998.

Singh V, Kaul S, Chander R, Kapoor NK: Stimulation of low density lipoprotein receptor activity in liver membrane of guggulsterone treated rats. Pharmacol Res 22(1):37-44, 1990.

Sirtori CR, Crepaldi G, Manzato E, et al: One-year treatment with ethyl esters of n-3 fatty acids in patients with hypertriglyceridemia and glucose intolerance: reduced triglyceridemia, total cholesterol and increased HDL-C without glycemic alterations. Atherosclerosis 137(2):419-27, 1998.

Staprans I, Pan XM, Rapp JH, Feingold KR, Jenkins DJ, Wolever TM, Kalmusky J, et al: Low-glycemic index diet in hyperlipidemia: use of traditional starchy foods. Am J Clin Nutr 46:66-71, 1987.

Stefanick ML, Mackey S, Sheehan M, Ellsworth N, Haskell WL, Wood PD: Effects of Diet and Exercise in Men and Postmenopausal Women with Low Levels of HDL Cholesterol and High Levels of LDL Cholesterol. N Engl J Med 339(1):12-20, 2 July 1998.

Stephen MacMahon, Norman Sharpe, Greg Gamble, Hamish Hart, John Scott, John Simes, Harvey White: Effects of Lowering Average or Below-Average Cholesterol Levels on the Progression of Carotid Atherosclerosis: Results of the LIPID Atherosclerosis Substudy. Circulation 97:1784-1790, 1998.

Tertov VV, et al: Antioxidant content in low density lipoprotein and lipoprotein oxidation in vivo and in vitro. Free Radic Res 29(2):165-73, Aug 1998.

Tertov VV, et al: Characteristics of low density lipoprotein isolated from circulating immune complexes. Atherosclerosis 122(2):191-9, May 1996. The Lancet, 27 March 1999.

Turpeinen AN, W-J, Aro A, Lorenz R, Mutanen M: Similar Effects of Diets Rich in Stearic Acid or trans-Fatty Acids on Platelet Function and Endothelial Prostacyclin Production in Humans. Arterioscler Thromb Vasc Biol 18:316-322, 1998.

van de Vijver LPL, Kardinaal AFM, van Duyvenvoorde W, Kruijssen DACM, Grobbee DE, van Poppel G, Princen HMG: LDL Oxidation and Extent of Coronary Atherosclerosis. Arterioscler Thromb Vasc Biol 18:193-199, 1998.

Vega GL, et al: Hypoalphalipoproteinemia (low high-density lipoprotein) as a risk factor for coronary heart disease. Curr Opin Lipidology 7:209-216, 1996.

WH Howell, DJ McNamara, MA Tosca, BT Smith, JA Gaines: Plasma lipid and lipoprotein responses to dietary fat and cholesterol: a meta-analysis. Am J Clin Nutr 65:1747-1764, 1997.

Willett WC, et al: Trans fatty acids: are the effects only marginal? American Journal of Public Health 84:722-724, 1994.

Wolfe BM: Potential role of raising dietary protein intake for reducing risk of atherosclerosis. Can J Cardiol 11(supp G):127G-131G, 1995.

Wu YJ, Hong CY, Lin SJ, Wu P, Shiao MS: Increase of Vitamin E Content in LDL and Reduction of Atherosclerosis in Cholesterol-Fed Rabbits by a Water-Soluble Antioxidant-Rich Fraction of Salvia miltiorrhiza. Arterioscler Thromb Vasc Biol 18:481-486, 1998.

Yudkin J: Sucrose and cardiovascular disease. Proc Nutr Soc 31:331-337, 1972

© Copyright 2002 Michael Lam, M.D. All Rights Reserved.


Understanding cholesterol: The good and the bad

DrLam.com
5 -
Thank you, Dr. Lam, for your excellent website.
 
I am a sixty-nine year old woman trying to balance my hormones due to "unexplained" minor bleeding, off and on for a long time now... years. I have never taken BC pills and I have always refused HRT except for bio- identicles for 8 or 9 months, which may have made my problems worse instead of better. This you explained well in your article, Estrogen Dominance. Thank you!
 
This morning I realized that my hormone balancing "problems" started about the time I was talked into taking a Statin for "high cholesterol" which I continue to take each day. Now understanding that cholesterol is necessary for hormones to do be made and do their jobs correctly, I wonder if reducing cholesterol in a (woman's) body doesn't set her (me) up for a hormone up-set? I want to stop my Statin (as well as further tweaking my diet), give it about 2 months and see if my symptoms decrease. I plan to see my doctor tomorrow and to tell him of my decision. Thoughts?