Middle-age men and women who have cardiovascular issues, such as high cholesterol and high blood pressure, may not only be at risk for heart disease, but for an increased risk of developing early cognitive and memory problems as well. That’s according to a study released today that will be presented at the American Academy of Neurology’s 63rd Annual Meeting in Honolulu April 9 to April 16, 2011.

For the study, 3,486 men and 1,341 women with an average age of 55 underwent cognitive tests three times over 10 years. The tests measured reasoning, memory, fluency and vocabulary. Participants received a Framingham risk score that is used to predict 10-year risk of a cardiovascular event. It is based on age, sex, HDL cholesterol, total cholesterol, systolic blood pressure and whether they smoked or had diabetes.

The study found people who had higher cardiovascular risk were more likely to have lower cognitive function and a faster rate of overall cognitive decline compared to those with the lowest risk of heart disease. A 10-percent higher cardiovascular risk was associated with poorer cognitive test scores in all areas except reasoning for men and fluency for women. For example, a 10 percent higher cardiovascular risk was associated with a 2.8 percent lower score in the test of memory for men and a 7.1 percent lower score in the memory test for women.

Higher cardiovascular risk was also associated with a 10-year faster rate of overall cognitive decline in both men and women compared to those with lower cardiovascular risk.

“Our findings contribute to the mounting evidence for the role of cardiovascular risk factors, such as high cholesterol and blood pressure, contributing to cognitive problems, starting in middle age,” said study author Sara Kaffashian, MSc, with INSERM, the French National Institute of Health & Medical Research in Paris. “The study further demonstrates how these heart disease risk factors can contribute to cognitive decline over a 10-year period.”

Source: American Academy of Neurology (AAN)
Cholesterol From Medical News Today

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Soy protein’s ability to lower total and LDL (low-density lipoprotein or “the bad”) cholesterol has been extensively studied, but the mechanism whereby soy protein lowers cholesterol remains unresolved. A new study published in the Journal of Clinical Lipidology last month shows that soy protein lowers total cholesterol and non-HDL (non-high-density lipoprotein) cholesterol significantly more than milk protein in patients with moderately high cholesterol levels.

“Non-HDL cholesterol has been shown to be a somewhat stronger predictor of cardiovascular disease and mortality risk than LDL cholesterol in population studies,” said Elaine Krul, co-author of the study and nutrition discovery lead at Solae. “The fact that soy protein significantly decreased non-HDL cholesterol levels compared to milk protein in this study is very promising.”

This randomized, controlled, parallel arm trial evaluated the effects of an insoluble fraction of soy protein, compared to total milk proteins with high calcium content, on the fasting lipid profile. It also assessed the potential contributions of increased excretion of bile acids and neutral sterols to their lipid-altering effects.

“The results of this study also showed that soy protein lowered non-HDL through a mechanism that does not involve increased bile acid excretion, but some yet to be determined mechanism,” said Kevin Maki, lead author of the study. “Nonetheless, these results are supportive of the heart health claim for soy protein.”

The Food and Drug Administration (FDA) heart health claim for soy protein established in 1999 states that “25 grams of soy protein a day, as part of a diet low in saturated fat and cholesterol, may reduce the risk of heart disease.” Currently, 11 other countries have approved health claims for soy protein’s potential to lower blood cholesterol and lower the risk of coronary heart disease.

Solae’s soy protein that was used in this study was a relatively insoluble fraction of soy protein isolate that had been shown to lower plasma cholesterol and increase fecal bile acid excretion in animals. The levels of isoflavones in the soy protein were lower than the average commercial soy protein isolate further supporting the notion that isoflavones do not play a role in the cholesterol lowering. The milk protein supplemented group also showed a modest cholesterol lowering.

Subjects for this study included men and women 18 to 79 years of age with elevated cholesterol, defined as fasting LDL-cholesterol concentrations of at least 100 mg/dL and less than 200 mg/dL while receiving no lipid altering therapy. Once recruited, participants were asked to follow a Therapeutic Lifestyle Changes diet throughout the study. Subjects that still met the inclusion criteria were then screened for their ability to lower their cholesterol in response to a bile acid binding drug, colesevelam. A majority of subjects responded and were then randomized to the test protein groups.

Source:
Jennifer Starkey
Solae, LLC

Cholesterol From Medical News Today

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The researchers, from Columbia University College of Physicians & Surgeons, New York, NY, report their investigation in a study published in the December issue of Archives of Neurology, a JAMA/Archives journal.

Low levels of high-density lipoproteins (HDL), a well-known risk factor for heart disease, are common in the US, said lead author Dr Christiane Reitz, assistant professor of neurology in the Sergievsky Center and Taub Institute at the University, in a press statement.

She and her colleagues also wrote in their background information that:

“Dyslipidemia [high total cholesterol and triglycerides] and late-onset Alzheimer’s disease are highly frequent in western societies.”

“More than 50 percent of the US adult population has high cholesterol. About 1 percent of people age 65 to 69 years develop Alzheimer’s disease, and the prevalence increases to more than 60 percent for people older than 95 years,” they added.

Previous studies of HDL and Alzheimer’s risk have either found no link or their findings have been unclear, but their new study followed participants for longer, resulting in a more accurate account of the numbers who went on to develop Alzheimer’s disease, the researchers told the press.

For this study, for an average of four years, they followed 1130 elderly people living in northern Manhattan. The participants came from a random sampling of Medicare recipients and were aged 65 and over. None had a history of dementia or cognitive impairment when they joined.

To collect their data, Reitz and colleagues studied medical, neurological and neuropsychological evaluations.

They assigned a diagnosis of “probable” Alzheimer’s disease when onset of dementia could not be explained by any other disorder and a diagnosis of “possible” Alzheimer’s disease when the most likely cause of dementia was Alzheimer’s disease but there was evidence that other disorders could have contributed to the dementia, such as stroke or Parkinson’s disease.

The researchers found that:

• Over the follow up, 101 participants developed Alzheimer’s, of which 89 were “probable” and 12 were “possible”.
• The mean age of participants who received either of these diagnoses was 83 years at onset.
• They were also more often Hispanic and had a higher prevalence of diabetes at the start of the study than counterparts who did not develop dementia.
• Higher blood levels of HDL (above 55 mg/dl) were linked with a decreased risk of both probable and possible Alzheimer’s, even after adjusting for vascular risk factors and lipid-lowering treatments.
• Adjusting for vascular risk factors and lipid-lowering treatments eliminated any links between higher total cholesterol, non-HDL cholesterol and LDL cholesterol levels and risk of probable and possible Alzheimer’s disease.
• There was a 40 per cent higher rate of developing Alzheimer’s among those with low HDL (below 55 mg/dl).

Reitz and colleagues concluded that in this study:

” … higher levels of HDL cholesterol were associated with a decreased risk of both probable and possible Alzheimer’s disease.”

They also noted it was important to consider, when interpreting these results, that the study was “conducted in an urban multiethnic elderly community with a high prevalence of risk factors for mortality and dementia.”

“Thus, our results may not be generalizeable to cohorts with younger individuals or to cohorts with participants with a lower morbidity [disease] burden,” they stressed.

Nonetheless, a distinguishing feature of this study is that unlike previous studies that included mostly white people, it included a large number of African Americans and Hispanics, suggesting the link between low HDL and higher risk of Alzheimer’s may apply in many different ethnic groups.

Speculating on their results, Reitz told the press it is not clear why HDL may be linked to higher risk of Alzheimer’s, but said there was some evidence to suggest two reasons:

“We know low HDL raises the risk of stroke and that stroke is associated with Alzheimer’s”, said Reitz, “so stroke may be the mediator”.

“But there’s also evidence that HDL works by itself to clear amyloid proteins from the brain,” she added.

Alzheimer’s is thought to be caused by two abnormal structures found in the brains of people who have died of the disease: plaques and tangles. The plaques are deposits of amyloid beta proteins that build up in the spaces between brain cells, tangles are twisted fibers of tau protein that build up inside cells.

According to the Alzheimer’s Association, there are 5.3 million Americans living with Alzheimer’s disease. From 2000 to 2006, Alzheimer’s disease deaths increased 46.1 per cent, while other major causes of death like prostate cancer, breast cancer, heart disease HIV-related illnesses, and stroke decreased.

The Association says strategic investments in other diseases have led to decline in deaths, and the same type of investment is urgently needed for Alzheimer’s.

“If raising HDL can lower a person’s risk of developing Alzheimer’s disease, that means we may be able to significantly reduce the rate of Alzheimer’s disease in the population.” said Reitz, adding that their findings now need to be confirmed by other studies.

Grants from the National Institute on Aging, the Charles S Robertson Memorial Gift for Research in Alzheimer’s Disease and the Blanchette Hooker Rockefeller Foundation helped pay for the study.

Cholesterol News From Medical News Today

Their study, the first to show such an association, is published in the December issue of The American Journal of Pathology. It demonstrates how mice eating a Western diet, and predisposed to develop prostate cancer, can develop larger tumors that are faster growing and metastasize more easily to the lungs, compared to animals eating a control diet.

In this study, a research team led by Philippe G. Frank, Ph.D., assistant professor in the Department of Stem Cell Biology and Regenerative Medicine at Jefferson, tried to understand why prostate cancer incidence is low in Asian countries, but significantly increases in Asian men who move to the United States. “Our hypothesis is that environmental factors, most likely present in the diet, may act as late stage promoters, responsible for the transformation of a prostate tumor from an early stage form into a more aggressive and clinically-apparent form,” says Dr. Frank.

Dietary fat and cholesterol have been shown to be risk factors in the development and progression of other tumor types, but diet-based studies in prostate cancer patients have reached contradictory conclusions, Dr. Frank says. For this reason, he and his colleagues turned to the TRAMP transgenic mouse model to determine the role of dietary fat and cholesterol. This mouse model is believed to closely parallel the pathogenesis of human prostate cancer.

TRAMP mice were placed on a diet that contained 21.2 percent fat and 0.2 percent cholesterol, reflective of a typical Western diet. A control group of TRAMP mice was fed a normal chow that had 4.5 percent fat and negligible amounts of cholesterol.

They found that the Western diet accelerated prostate tumor development and progression. These tumors also produced increased levels of receptors that bind to lipoproteins carriers of cholesterol, and they were more aggressive. The researchers further discovered that the TRAMP mice fed a Western diet appeared to experience greater incidence of cancer metastasis to the lungs, compared to the control group.

The research team also noted that TRAMP mice fed the high fat/high cholesterol chow had less cholesterol in their blood compared to control mice fed the same diet. “This likely reflects the fact that their tumors depend on cholesterol to grow,” explains Dr. Frank. “This study suggests that monitoring cholesterol levels in men at risk, diagnosed, or treated for prostate cancer may help limit cancer growth or even recurrence.”

Dr. Frank says the evidence involving cholesterol is strong – a finding he believes makes sense physiologically. “Cells need cholesterol to produce androgen hormones, and androgen hormones promote prostate cancer growth,” he explains. “Perhaps more importantly, we also believe that tumors feed on cholesterol, and the more blood cholesterol is accessible, the more is available for tumor growth.

“Although this is a mouse study, numerous studies have shown the health benefits of controlling blood cholesterol levels and fat intake. This research suggests the same advice may offer some benefit for men at risk of developing prostate cancer or even diagnosed with prostate cancer,” says Dr. Frank.

He adds statins that lower cellular cholesterol production may be one way to reduce prostate cancer progression – although that has yet to be demonstrated. Monitoring blood cholesterol levels of prostate cancer patients may also provide important information about cancer progression. “For example, tests showing a sudden drop in blood cholesterol is often indicative of the development of tumors,” Dr. Frank adds.

Dr. Frank receives funding from the Jane Barsumian/Mary Lyons Trust and the Susan G. Komen Foundation; the first author, Gemma Llaverias Ph.D., was supported by the Spanish Ministry of Science and Innovation. The other study co-authors are Christiane Danilo, M.S., Yu Wang, M.S., Agnes Witkiewicz, M.D., Kristin Daumer, M.S., and Michael Lisanti, M.D., Ph.D.

All researchers are from Thomas Jefferson University, are affiliated with the Kimmel Cancer Center, and declare no conflicts of interest.

Cholesterol News From Medical News Today

Determining the EFficacy and Tolerability of CETP INhibition with AnacEtrapib (DEFINE) is a randomized, double-blind trial of 1,623 patients who took either 100 milligrams (mg) of the cholesterylester transfer protein (CETP) inhibitor anacetrapib, or a placebo for 18 months at 153 centers in 20 countries. The patients were already being treated with a statin and/or other lipid-lowering medicine and had achieved their goal level of low-density lipoprotein (LDL) cholesterol.

The study’s primary endpoints were the percent change in LDL, known as the “bad” cholesterol associated with the development of clogged arteries, and safety as measured by a number of clinical and laboratory measures as well as cardiovascular (CV) events.

Anacetrapib reduced LDL by 40 percent – from 81 milligrams per deciliter (mg/dL) to 49 mg/dL. It also more than doubled the level of high-density lipoprotein cholesterol (HDL) that helps clear lipids from the bloodstream – from 40 mg/dL to 101 mg/dL – without raising blood pressure.

“Anacetrapib has a knock-your-socks-off effect on HDL and a jaw-dropping effect on LDL,” said Christopher P. Cannon, M.D., senior investigator of the TIMI Study Group in the cardiovascular division of Brigham and Women’s Hospital in Boston, Mass. “These changes are striking because virtually all the patients in the study were already taking cholesterol-lowering drugs and achieved previously unattainable levels of good and bad cholesterol.”

The experimental drug is one of a new class that blocks the ability of the CETP enzyme to transfer cholesterol particles from the good HDL to the bad LDL.

Elevated LDL and low levels of HDL are both risk factors for cardiovascular disease. Statins reduce LDL and lessen cardiovascular risk. Despite statin therapy, many patients still have a high risk of cardiovascular disease.

High natural levels of HDL are associated with lower cardiovascular risk, which is why researchers have been looking for ways to increase HDL levels, said Cannon, an associate professor of medicine at Harvard Medical School.

“No treatments raise HDL levels as substantially as seen here (more than doubling of the levels),” said Cannon.

Patients in DEFINE were 62.5 years old on average; 23 percent were women; 17 percent were Asian, black or multiracial and 15 percent were Hispanic. The study included interim safety analyses at six and 12 months, and researchers found no change in blood pressure or electrolytes among participants.

Levels of aldosterone, a hormone produced in the adrenal gland that affects kidney function and blood pressure, didn’t change. The researchers also found no increase in muscle problems or liver function abnormalities between groups – a side effect occasionally associated with statins.

Although the study was not designed or powered to assess the effects of anacetrapib on cardiovascular events, fewer cardiovascular events occurred in the anacetrapib group than in the statin-only group. The full efficacy and safety of anacetrapib will be evaluated in a larger Phase III trial, Cannon said.

“This agent provides us a very strong add-on treatment to statins that dramatically increases the good cholesterol and dramatically further decreases the bad cholesterol,” he said. “If the cardiovascular effects are borne out by future research, it would be a very promising approach to reducing cardiovascular events in patients with or prone to atherosclerosis.”

Co-authors are Sukrut Shah, R.Ph., Ph.D.; Hayes M. Dansky, M.D.; Michael Davidson, M.D.; Eliot A. Brinton, M.D.; Antonio M. Gotto Jr., M.D., D.Phil.; Michael Stepanavage, M.S.; Sherry Xueyu Liu, M.S.; Patrice Gibbons, M.S.; Tanya B. Ashraf, B.A.; Jennifer Zafarino, M.S.; Yale Mitchel, M.D. and Philip Barter, M.D., Ph.D. Author disclosures are on the abstract.

Merck Research Laboratories, Rahway, N.J., funded the study.

Cholesterol News From Medical News Today

Alzheimer’s disease is a severe neurodegenerative disorder of the brain that is characterized by loss of memory and cognitive decline. The majority of Alzheimer’s disease cases are sporadic (risk age >60 years), and only <2.5% have a genetic disposition. It is estimated that in 2050, approximately 80 million people will suffer from Alzheimer’s disease worldwide. The major pathological hallmarks of Alzheimer’s disease are extracellular aggregates (plaques) of the small peptide beta-amyloid, hyperphosphorylation of the protein tau and subsequent formation of intracellular neurofibrillary tangles, degeneration of neurons secreting the neurotransmitter acetylcholine, inflammation, and cerebrovascular dysfunction.

The causes for Alzheimer’s disease are not known, but dysregulation of amyloid-precursor protein expression and beta-amyloid clearance is hypothesized (beta-amyloid cascade). Alternatively, a pathological cascade of events may trigger hyper-phosphorylation of tau, putting the tau-hypothesis into the center. A third hypothesis suggests that chronic long-lasting mild cerebrovascular damage, including inflammatory processes and oxidative stress, may cause Alzheimer’s disease. It has been suggested that Alzheimer’s disease starts 20-30 years before first symptoms appear and recent studies have shown, that high cholesterol levels are linked to the pathology of this disease.

The aim of the study led by Humpel was to study the effects of hypercholesterolemia in adult rats. Male 6 months old Sprague Dawley rats were fed with normal food (controls) or with a special 5% cholesterol-enriched diet (hypercholesterolemia). After 5 months animals were tested for behavioral impairments and pathological markers similar to those found in the brains of patients with Alzheimer’s disease. The results showed that chronic hypercholesterolemia caused memory impairment, cholinergic dysfunction, inflammation, enhanced cortical beta-amyloid and tau and induced microbleedings, all indications, which resemble an Alzheimer’s disease-like pathology.

Thus the data are in line with earlier studies showing that high fat lipids, including cholesterol, may participate in the development of sporadic Alzheimer’s disease. However, since Alzheimer’s disease is a complex heterogenous disease, these data do not allow the conclusion that cholesterol alone is responsible for the disease. It can be speculated that chronic mild cerebrovascular damage caused and potentiated by different vascular risk factors (including cholesterol) may contribute to these pathologies. It needs to be determined in future studies how mild chronic microvascular bleedings, silent strokes and mild blood-brain barrier damage over decades may play a role in the development of this disease. Indeed several data (Ladecola, Nat.Rev.Neurosci. 5, 347-360, 2004) support the view that Alzheimer’s disease can be considered as a vascular disease and that a dysfunctional clearance of beta-amyloid from brain to blood and vice versa may be a secondary important step in the cascade of initiation of the disease.

Cholesterol News From Medical News Today

Led by Angel Baldán, Ph.D., assistant professor of biochemistry and molecular biology at Saint Louis University and published in a recent issue of Proceedings of the National Academy of Sciences of the United States of America, the study found that the microRNA miR-33, may be key to controlling HDL, or “good” cholesterol levels.

In the U.S., heart attack, stroke, and peripheral artery disease collectively account for more than 30 percent of all deaths in the last decade. Atherosclerosis, the fatty build-up in arteries that causes these illnesses, is tied to cholesterol levels, a waxy substance found in the blood.

Statins, drugs frequently prescribed by doctors to manage cholesterol levels, work by lowering LDL, or “bad” cholesterol levels; however, their role in HDL cholesterol is still obscure. Importantly, HDL has been found to have a protective benefit against cardiovascular disease.

“Atherosclerosis costs lives and takes an enormous toll on our health,” said Baldán. “If the discovery that miR-33 can be used to raise HDL levels leads to better medications, it will have an enormous impact on our ability to treat heart disease.”

The study, which was funded by the National Institutes of Health, Saint Louis University Center for Cardiovascular Research and the Doisy Department of Biochemistry and Molecular Biology at Saint Louis University, examined SREBP-2, an important gene in the body, and zeroed in on the microRNA miR-33, which is expressed within SREBP-2.

Increasing the levels of miR-33 in the liver, scientists discovered, resulted in lower HDL cholesterol levels in an animal model; conversely, turning off miR-33, researchers found, had the effect of raising HDL levels.

Paralleling these results, four separate studies reported similar findings, adding to investigators’ hope that better medications may be on the horizon for managing atherosclerosis. Scientists hope that future medications may prove to be more effective than statins alone by not only lowering LDL-cholesterol levels, but also increasing HDL levels.

Cholesterol News From Medical News Today

The biggest culprit of high cholesterol is undoubtedly our daily diet. A diet high in saturated fat is a sure fire way to increase LDL cholesterol and put ourselves at risk for heart disease, clots, stroke and, left untreated, even death.

It is essential that you not only learn how to lower LDL cholesterol, but you incorporate what you learn into your daily life.

Modifying your daily diet to reduce foods high in saturated fats, like dairy products and red meats, will definitely help lower cholesterol. Biscuits, cakes, cheese, spreads, pork, beef, lamb etc., when overused, contribute to high cholesterol.

Adding more fruits, vegetables and foods like peas, beans and oat bran, which are rich in dietary fibre, will all answer the how to lower LDL cholesterol question.

Adding or increasing physical exercise is another natural way to lower bad cholesterol. Start off slowly, especially if you have not exercised for a while. The worse thing you can do is go off all guns blazing on some mad exercise routine! For one, you will never sustain this, and two, you will probably injure yourself.

Our bodies need nutrients, and what with all the health scares we have had, bird flu, swine flu, mad cow disease, to name but a few, we are no longer certain of what nutrients we are really getting in our daily diet.

To this end, when I carried out my in depth research on how to lower LDL cholesterol, as a long time sufferer of high cholesterol, I specifically looked into what natural supplements were available to aid this process and sustain it long term.

Any natural supplement used to lower cholesterol, absolutely, without doubt, must have the best of the best of proven nutrients. This is absolutely imperative. There are so many gimmicky supplements out there on the marketplace, which fail to deliver on how to lower LDL cholesterol, and in some cases, cause adverse side effects in other areas of our bodies.

LDL cholesterol is not something to be messed around with or ignored. It is serious. The question is, how serious are you about dealing with it?

The liver combines cholesterol with lipoproteins for use in various physiological body functions and building of tissues. A lipoprotein is a combined unit of lipid, that is, fat on the inside surrounded by protein on the outside.

What are Lipoproteins?
Since cholesterol is water-insoluble, the blood cannot carry it unless it is turned into a water-soluble form. That is where water-soluble lipoproteins enter the scene. They combine with cholesterol to form water-soluble units that can move through the bloodstream.

These lipoproteins are mainly of two types: low-density (20-25% proteins) lipoproteins, LDL and high-density (40-55% protein) lipoproteins, HDL. Medical experts refer to the cholesterol transported by HDL as HDL cholesterol.

So What is HDL?
So, when medical experts talk of HDL cholesterol, they mean HDL-bound cholesterol. Scientifically speaking there is no such thing as “good cholesterol” or “bad cholesterol”. Cholesterol is just cholesterol, a sterol lipid having the chemical formula C27H45OH. In fact, HDL and LDL are not cholesterol at all. They are just lipoprotein vehicles for carrying and moving cholesterol through blood.

Most people commonly call HDL good cholesterol because it travels from the arteries and body tissues back to the liver for recycling or elimination. This prevents a build-up of plaque (a hard fatty deposit) on the inner walls of major arteries supplying blood to the organs. This reduces clogging of the arteries and the risk of heart attacks, paralysis, and hypertension.

Recent Discovery
Scientists have recently discovered that low HDL cholesterol level in blood is an independent risk factor for these cardiovascular and crebrovascular diseases. HDL levels below 40 mg/dL for men and below 50 mg/dL for women are considered low. This is separate from the total cholesterol and LDL levels. This means that even with a normal total cholesterol count and a safe LDL level, people with low HDL cholesterol levels are at an increased risk of heart disease.

Why Lowering Cholesterol Is Not Important
So the emphasis should not only be on lowering the total cholesterol and LDL levels, but also raising the HDL cholesterol level. Research has shown that a drop of just 1 mg/dL in the HDL cholesterol level can lower a person’s risk of suffering a fatal heart attack by 3%.

But how does one raise the HDL cholesterol level while keeping the total cholesterol and LDL levels low? Ideally, an HDL more than 50 mg/dL for men and 60 mg/dL for women is considered heart-protective. Most people, however, can push the HDL cholesterol levels up by making some lifestyle and diet changes.

Benefits of Raising Cholesterol
To raise your HDL cholesterol, take up an aerobic activity like walking, cycling, swimming or dancing for 30-40 minutes 5 times a week. Quitting smoking, losing excess weight and consuming foods rich in dietary soluble fiber, omega-3 fatty acids and antioxidants also raises the HDL cholesterol levels.

Another lifestyle change that is effective in raising HDL cholesterol is saying no to saturated and trans fats (red meats, egg yolk, butter, whole-cream dairy products, commercial bakery items, deep-fried foods, and so on). Instead go for a diet based on polyunsaturated and monounsaturated vegetable oils, whole grains, cereals, nuts like almonds and walnuts, flaxseeds, beans, legumes, lentils, fruits and vegetables.

The only drugs known to raise HDL cholesterol effectively are niacin (vitamin B3) and a class of compounds called fibrates.

High Density Lipoprotein is a substance that carries cholesterol particles from your artery walls back through the bloodstream and into the liver where some of it is metabolized and some excreted from your body in the form of bile salts. Statistics show that when the ratio is favorable, your risk of heart problems is minimized, so it makes sense to learn how to increase HDL, and keep the HDL LDL ratio as good as possible.

The ratio is determined by taking your LDL, (low-density cholesterol) number, and dividing it by your HDL (high-density cholesterol) number. The result is what doctors use to determine your risk of cardiovascular disease.
The higher the HDL, the lower the risk. Lets look at some numbers to give you an idea of how this works.

For example:

• Total cholesterol is: 200
• HDL is: 50
• LDL is: 150

The ratio would be: 3 This would be considered a good ratio, indicating the person would have a lower than average risk of heart disease.

Over time, what was considered to be good or safe levels of cholesterol have been adjusted downward, in part due to the push to get more people on cholesterol lowering medications. Foods to raise HDL have not been emphasized for this reason. The current medical model for prevention of cardiovascular disease focuses on drug therapy. This is why you must learn how to increase HDL and get the optimal HDL LDL ratio to prevent heart disease.

High-density lipoproteins have recently been found to have potent antioxidant activity, and this may well be the reason for its “protective” role in regards to vascular disease. See the notation below:

Vohl MC, Neville TA, Kumarathasan R, Braschi S, Sparks DL: A novel lecithin-cholesterol acyltransferase antioxidant activity prevents the formation of oxidized lipids during lipoprotein oxidation. Biochemistry; 1999 May 11;38(19):5976-81

Several things that are known to raise HDL levels.

• Aerobic or interval training exercise
• Dietary changes – with balanced fat intake
• Eat for your blood type and metabolic type
• Specific nutritional supplements

The foods to increase HDL do it in several ways. Some foods like healthy fats, provide the raw materials or (precursors) your body needs to make HDL. Other foods such as high fiber foods and low glycemic fruits and vegetables may indirectly raise HDL by preventing inflammation, boosting antioxidant status, and lowering blood sugar and insulin. Some of these foods may also possess antioxidant activity themselves and work synergistically with HDL to protect against cardiovascular disease.

Specific supplements that will raise HDL levels and help optimize the HDL LDL ratio are:

• Fish oil
• Pantothenic acid (vitamin B-5)
• niacin – (vitamin B-3)
• Gugulipid
• Coenzyme Q-10
• Carnitine
• Vitamin-C
• Magnesium
• Polycosanol
• Vitamin E-complex
• Alpha Lipoic Acid
• N-Acetyl-Cysteine
• CLA – conjugated linoleic acid

All of these supplements help increase HDL levels, however niacin (B-3) and calcium pantothenate (B-5) are the most effective. Focus on them first, and add others if needed.

Foods to Raise HDL

There are a number of foods that are claimed to raise HDL levels. Among these are:

• Fatty fish such as salmon, tuna, mackerel, sardines
• Raw nuts and seeds such as walnuts, pecans, almonds, and flaxseeds
• Whole eggs
• Onions
• Fresh raw low glycemic vegetables – especially dark leafy greens
• Oat bran
• Alcohol – 1 or 2 drinks per day maximum

Action Steps

• Get your HDL LDL ratio tested to establish baseline levels
• Work in 3 sessions of circuit weight training or interval training per week
• Eat for your blood type and metabolic type
• Avoid of refined foods as possible – stick to raw fruits and vegetables
• Be sure to get plenty of good fats in your daily diet
• Supplement with niacin (B-3) and calcium pantothenate (B-5) to raise HDL

The HDL LDL ratio is one of the cornerstones of wellness and antiaging. It’s a benchmark that will help you really reduce your risk of heart disease and ensure a long and healthy life!