Functional Health Services for Your Well Being

is it good to be a chinese vegetarian?

November 5th, 2012

Many studies have shown that vegetarian diet has beneficial effects on the prevention of cardiovascular diseases. However, the effect of vegetarian diet on carotid intima-media thickness (IMT), as well as the association between IMT and duration of vegetarian diet, are still unclear. The present study aims to investigate the influence of duration of vegetarian diet on cardiovascular risk factors, and more importantly on IMT among Chinese vegetarians, that do they best to keep up their weight, although some of them go for cosmetic procedures which you can get online to look better in your clothes as well. Methods: One hundred and seventy-one Chinese male vegetarians were screened for metabolic profile, cardiovascular risk and carotid IMT. They were compared with 129 age-matched omnivores recruited from a community-based health project. The effects of confounding factors were adjusted by stepwise logistic regression analysis. Results: Compared to the omnivores, the vegetarians had lower BMI, weight, systolic blood pressure and diastolic blood pressure. Also, the levels of triglyceride, total cholesterol, HDL-Cholesterol, LDL-Cholesterol, ApoA1, ApoB, uric acid, albumin and gamma-glutamyltransferase were significantly reduced in vegetarians. Omnivores had significantly higher fasting blood glucose than that of vegetarians. However, there were no differences in fasting insulin, C-reactive protein and HOMA-IR between the two groups. IMT was thinner in the vegetarian group than in the omnivore group (0.59 +/- 0.16 vs. 0.63 +/- 0.10 cm, P < 0.05). The vegetarians were divided according to duration of vegetarian diet (< 6 years, 6 to [less than or equal to]11 years, >11years), those in tertile 1 (< 6 years) and tertile 2 (6 to [less than or equal to]11 years) had shown thinner IMT as compared to the omnivores, and tertile 3 had shown no reduction. Conclusion:A decrease in multiple cardiovascular risk factors such as BMI, blood pressure and lipid profile was associated with vegetarian diet. Moreover, taking a low-calorie, low-protein, or vegetarian diet might have great beneficial effects on IMT through improved lipid profile, and the beneficial effects appeared to be correlated with the duration of vegetarian diet

Take that with a grain of salt

July 14th, 2012

Is Salt Really as Bad as THEY Say it is?

by Alex Boersma

We all know that salt is bad for you.  We’ve heard it since we were kids.  Most of us can probably remember our mothers taking the salt shaker away from our pot-bellied fathers, chastising them for risking their lives by putting SALT on their food.  Today, the venerable salt shaker has gone missing from the every-day dinner table.  Sure, it still makes the occasional guest appearance at Thanksgiving and Christmas dinner, but even then, we try to put our hands on it only when nobody else is looking.

Most people accept as a given that salt consumption causes high blood pressure and heart disease.  As somewhat of a health skeptic, I have for some time had concerns about the certainty with which this salt – blood pressure – heart disease link is proclaimed.  But because of the strength of the consensus on salt and the lack of solid evidence refuting said link, I have kept my reservations to myself.  In the past year, however, the controversy over salt has reached a crescendo in the medical journals and has even spilled over into the more mainstream media.  It is time to come out of the salt closet and take a stand.  It is time to give the salt – blood pressure – heart disease hypothesis the licking it deserves. Read the rest of this entry »

beach body at 90

June 10th, 2012

by Alex Boersma

If you read just about any text on the physiology of ageing you will quickly come to the disheartening conclusion that sarcopenia (muscle loss) is the inevitable result of outliving your peers.  At 1 percent per year, the expected and accepted annual loss of muscle mass after age 40 condemns us to carry little more than skin on our bones if we are lucky enough to live into our 90’s. this is why people should keep on using the Rapid Tone Diet their whole life.  But don’t tell that to Charles Eugster:

90 year old beach body

At the ripe young age of 93, Charles continues to win masters rowing and body building championships despite what it says in the physiology texts.  He is a vibrant and compelling public speaker who’s 2012 TED talk, should be required viewing for anybody even considering a sedentary retirement.  His lifestyle is a paragon of active living and the antithesis of what we accept as normal ageing.  If ever there was someone who could save Nike from the Lance Armstrong and Tiger Woods fiascos, it would be Charles. Imagine – instead of:

LIVESTRONG (but die young due to complications of performance enhancing drugs or taking a golf club up side of the head)

we could have:


I, for one, am excited to see a noctogenarian athlete in the headlines.  From personal experience, I know that those physiology texts have it all wrong.  In the 15 years since I started reading them I have significantly increased my own muscle mass and, most importantly, more than doubled my strength.  I have witnessed Jack Palance, at age 73, doing one arm push-ups at the acadamy awards. I have followed Jack Lalane as he performed feats of strength and endurance in his 70’s.  I have admired the insanity of Don Wildman’s decidedly youthful workouts. And I have watched carefully as “average people” such as Allan Johnson (below) continue to do, in their 80’s, things that most 40 year olds would never even dream of attempting.

allan johnson ropes cows at 83 don wildman

Allen Johnson roping cows at 83, Don Wildman paddle boarding at 76

I have also had the misfortune of observing as entire generations of potentially fit people morphed into jelly-bellied couch potatoes.  Now I’m not saying the physiology texts are responsible for the fattening of humanity, but they sure don’t help when they tell us we should expect a healthy serving of frailty with our CPP cheques!

The truth is, most people lose muscle and gain fat until they reach their seventies.  Most people, if they haven’t already died from the complications of a slothlike lifestyle, then usually begin to wither away until they die from old age or, as I like to call it, skin and bone disease.  In the meantime, for most people, quality of life and vitality often decline significantly as even the simplest chores become daunting obstacles, and that’s why many people decide to try other methods as cosmetic surgery with professionals as the Dr. Joseph Racanelli, to eliminate fat and be more attractive a and healthy.

But you don’t have to be most people!

What most of the physiology texts don’t tell you is that, for the most part, you control your strength and muscle mass.  There are a multitude of studies indicating that it is possible to significantly improve strength and muscle mass well into your octogenarian years.  This paper summarizes the results of many of those studies and concludes with:

Strength gains in response to resistance exercise training in the elderly, although substantial, may be less than in young individuals. Increases in muscle mass appear to be similar in elderly and young individuals as does the muscle protein synthetic response to resistance exercise. Muscle co-activation appears to be substantially and similarly reduced (improved) in young and elderly individuals as a result of resistance training.”St

Translated:  You can get very strong if you are old, although not as strong as if you had started when you were younger.  You can get just as muscular as a young person.  And you can learn to move just as efficiently as a young person, one great way for this is to start with Yoga workouts, to have a better flexibility and great strong muscles and a URBNFit Exercise Ball will help you if you want to try something different, effective and totally affordable from home.  You just have to put in some time at the gym lifting heavy stuff.  Here’s what you have to do:

  1. Lift weights.  Heavy weights.

Childhood Obesity

March 16th, 2012


by Alex Boersma

Make no mistake.  This is a rant.  If the heading above offends you, I suggest you stop reading now.  It ain’t gonna get any better!  But if you are genuinely concerned about your child’s weight, I suggest you tough it out.  You can and should be the one to save your child from the lifelong affects of battling with weight.  If you’re not going to do it, who will? Read the rest of this entry »

diabetes 3

January 22nd, 2012

Measuring Insulin Resistance

by Alex Boersma

In Part I of this series I described type II diabetes as the most pernicious and calamitous disease of the 21st century.  Indeed, it seems that despite modern advances in the  treatment of heart disease and cancer, the capability of our medical system to deal with blood sugar dysregulation remains pathetically inadequate.  In fact, just this week  Medscape reported on the 47th annual meeting of the European Association for the Study of Diabetes which described the diabetes epidemic as  ”on a relentlessly upward trajectory, with no signs of abating“.  From the meeting:

“Data from international studies demonstrate that the number of people withdiabetes in 2011 has reached 366 million. This year, 4.6 million deaths will be attributed to diabetes, with 1 person dying from diabetes every 7 seconds. Healthcare spending on diabetes has reached $465 billion, and people are not even getting treated how they should, sometimes it is better to opt for other care options like the one at”

And it’s not just in Europe.  Below is a chart from a  recent analysis of diabetes prevalence in Ontario

ontario diabetes statistics

 Follow the blue or red lines into the future and perhaps you’ll reconsider that venti frappucino if you plan on becoming a sexagenarian!

In Part II of the series, I examined the role of insulin resistance as a determining factor in the progression to type II diabetes.  Primary factors in the development of insulin resistance were discussed, including cellular accumulation of excess free fatty acids (FFA), stress, inflammation and fatty liver.  It was established that these four factors were  associated with each other in a cyclic fashion, meaning an increase in one factor frequently causes increases in other factors.  All four factors factors are clearly related to excess weight, particularly when that weight is carried predominantly in the abdominal area.

If insulin resistance is such a dominant risk factor in the progression to type II diabetes, it might be useful to have an effective tool for diagnosing it.  In this section I will discuss the various options available for measuring insulin resistance and their efficacy in predicting progression to type II diabetes. Read the rest of this entry »

inflammation and lifestyle

November 19th, 2011

Serhan and colleagues introduced the term “Resoleomics” in 1996 as the process of inflammation resolution. The major discovery of Serhan’s work is that onset to conclusion of an inflammation is a controlled process of the immune system (IS) and not simply the consequence of an extinguished or “exhausted” immune reaction. Resoleomics can be considered as the evolutionary mechanism of restoring homeostatic balances after injury, inflammation and infection. Under normal circumstances, Resoleomics should be able to conclude inflammatory responses. Considering the modern pandemic increase of chronic medical and psychiatric illnesses involving chronic inflammation, it has become apparent that Resoleomics is not fulfilling its potential resolving capacity. We suggest that recent drastic changes in lifestyle, including diet and psycho-emotional stress, are responsible for inflammation and for disturbances in Resoleomics. In addition, current interventions, like chronic use of anti-inflammatory medication, suppress Resoleomics. These new lifestyle factors, including the use of medication, should be considered health hazards, as they are capable of long-term or chronic activation of the central stress axes. The IS is designed to produce solutions for fast, intensive hazards, not to cope with long-term, chronic stimulation. The never-ending stress factors of recent lifestyle changes have pushed the IS and the central stress system into a constant state of activity, leading to chronically unresolved inflammation and increased vulnerability for chronic disease, so for this, visiting a chiropractic office helps a lot to alleviate these undesired effects. Our hypothesis is that modern diet, increased psycho-emotional stress and chronic use of anti-inflammatory medication disrupt the natural process of inflammation resolution ie Resoleomics.

We propose a model wherein chronic stress results in glucocorticoid
receptor resistance (GCR) that, in turn, results in failure to downregulate inflammatory response. Here we test the model in two
viral-challenge studies. In study 1, we assessed stressful life events,
GCR, and control variables including baseline antibody to the challenge virus, age, body mass index (BMI), season, race, sex, education, and virus type in 276 healthy adult volunteers. The volunteers
were subsequently quarantined, exposed to one of two rhinoviruses, and followed for 5 d with nasal washes for viral isolation
and assessment of signs/symptoms of a common cold. In study 2,
we assessed the same control variables and GCR in 79 subjects who
were subsequently exposed to a rhinovirus and monitored at baseline and for 5 d after viral challenge for the production of local (in
nasal secretions) proinflammatory cytokines (IL-1β, TNF-α, and IL-6).
Study 1: After covarying the control variables, those with recent
exposure to a long-term threatening stressful experience demonstrated GCR; and those with GCR were at higher risk of subsequently
developing a cold. Study 2: With the same controls used in study 1,
greater GCR predicted the production of more local proinflammatory cytokines among infected subjects. These data provide support
for a model suggesting that prolonged stressors result in GCR,
which, in turn, interferes with appropriate regulation of inflammation. Because inflammation plays an important role in the onset and
progression of a wide range of diseases, this model may have broad
implications for understanding the role of stress in health.


Sleep loss can occur as a result of habitual behavior or due to the presence of a pathological condition that is associated with reduced total sleep time. This column focuses on the impact of behavioral sleep curtailment, an endemic condition in modern society, and provides evidence against the old notion that “sleep is for the mind, and not for the rest of the body.”

Prevalence of Sleep Curtailment in Modern Society

Sleep curtailment is a hallmark of modern society, one that is often considered harmless and efficient. The advent of artificial light has permitted the curtailment of sleep to the minimum tolerable and an increase in the time available for work and leisure. In our 24-hour-a-day society, millions work during the night and sleep during the day, a schedule that generally results in substantial sleep loss.

Figure 1 illustrates changes in self-reported sleep duration over the past 50 years. In 1960, a survey of over 1 million people found a modal sleep duration of 8.0-8.9 hours.[1] In 2000, 2001, and 2002, polls conducted by the National Sleep Foundation indicated that the average duration of sleep for Americans had fallen to 6.9-7.0 hours.[2] Overall, sleep duration thus appears to have decreased by 1.5-2 hours during the second half of the 20th century. Today, many people are in bed only 5-6 hours per night on a regular basis.

Figure 1.


Self-reported sleep duration, 1960-2002.

The 2 major pathways by which sleep affects the release of hormones are the hypothalamic-pituitary axes and the autonomous nervous system.

The release of hormones by the pituitary — the “master” endocrine organ that controls the secretion of other hormones from the peripheral endocrine glands — is markedly influenced by sleep. Modulation of pituitary-dependent hormonal release is partly mediated by the modulation of the activity of hypothalamic-releasing and/or hypothalamic-inhibiting factors controlling pituitary function. During sleep, these hypothalamic factors may be activated — as in the case of growth hormone (GH)-releasing hormone — or inhibited, as is the case for corticotropin-releasing hormone.

The other pathway by which sleep affects peripheral endocrine regulation is via the modulation of autonomic nervous system activity. During deep sleep, sympathetic nervous system activity is generally decreased and parasympathetic nervous system activity is increased. Sleep loss is associated with an elevation of sympathovagal balance, with higher sympathetic but lower parasympathetic tone. Most endocrine organs are sensitive to changes in sympathovagal balance. Well-documented examples are pancreatic insulin secretion and release by the fat cells of leptin, an appetite-suppressing hormone.

A profound and generalized impact of sleep loss on the endocrine system should therefore be expected. Until recently, however, it was considered unlikely that the adverse effects of sleep deprivation on endocrine function would be long-term. The studies from which this notion was drawn examined the effects of only 1 or 2 nights of acute total sleep deprivation. In general, the data suggested that endocrine alterations that occurred during the sleepless night(s) were completely reversed during recovery sleep.

More recently, a few studies have examined the impact on hormones, metabolism, and immune function of the much more common, real-life situation — chronic partial sleep deprivation.[3-5] The earliest study measured hormonal and metabolic parameters in subjects studied after 6 days of sleep restriction (4-hour bedtime) and after full sleep recovery (6 days of 12-hour bedtime).[3] Subsequent studies examined the impact of less severe sleep restriction (6.5 hours per night) over 1 week[4] as well as the effects of short-term sleep curtailment (2 days with 4-hour vs 12-hour bedtime).[5]

Alterations of Pituitary-Dependent Hormones During Sleep Loss

The first effect of partial sleep loss on circulating levels of pituitary-dependent hormones to be documented under various study conditions is an increase in the early evening levels of the stress hormone cortisol.[3,6] Normally at that time of day, cortisol concentrations are rapidly decreasing to attain minimal levels shortly before habitual bedtime. The rate of decrease of cortisol concentrations in the early evening was approximately 6-fold slower in subjects who had undergone 6 days of sleep restriction than in subjects who were fully rested.[3] Elevations of evening cortisol levels in chronic sleep loss are likely to promote the development of insulin resistance, a risk factor for obesity and diabetes.

The upper and middle panels of Figure 2 illustrate the impact of sleep restriction on the thyroid axis.[3] After 6 days of 4-hour sleep time, the normal nocturnal thyroid-stimulating hormone (TSH) rise was strikingly decreased, and the overall mean TSH levels were reduced by more than 30%.[3] A normal pattern of TSH release reappeared when the subjects had fully recovered. Differences in TSH profiles between the 2 bedtime conditions were probably related to changes in thyroid hormone concentrations via a negative-feedback regulation, because the free thyroxine index (FT4I) was higher in the sleep-restriction condition than in the fully rested condition (middle panels of Figure 2). Thyroid axis function was thus markedly altered by partial recurrent sleep restriction.

Figure 2.


Levels of thyroid-stimulating hormone (TSH), free thyroxine index, and leptin in sleep-deprived vs well-rested subjects. From top to bottom, 24-hour (+SEM) profiles of TSH, free thyroxine indexes, and leptin in healthy young subjects when submitted to partial sleep restriction for 6 days (4-hour sleep times; mean total sleep time during previous 2 nights, 3 hours 49 minutes; left panels) and after full sleep recovery (12-hour sleep times for 6 nights; mean total sleep time during previous 2 nights, 9 hours 3 minutes; right panels). The black bars represent the sleep periods.[3,10]

The temporal organization of GH secretion is also altered by chronic partial sleep loss.[7] The normal single GH pulse occurring shortly after sleep onset splits into 2 smaller pulses, 1 before sleep and 1 after sleep; as a result, the peripheral tissues are exposed to high GH levels for an extended period of time, which, because GH has anti-insulin-like effects, could also have an adverse impact on glucose tolerance.

Impact of Sleep Loss on Hormones Controlling Appetite

Sleeping and feeding are intricately related. Animals faced with food shortage or starvation sleep less;[8] conversely, animals subjected to total sleep deprivation for prolonged periods of time increase their food intake markedly.[9] Recent studies in humans have shown that the levels of hormones that regulate appetite are profoundly influenced by sleep duration. Sleep loss is associated with an increase in appetite that is excessive in relation to the caloric demands of extended wakefulness.

The regulation of leptin, a hormone released by the fat cells that signals satiety to the brain and thus suppresses appetite, is markedly dependent on sleep duration. After 6 days of bedtime restriction to 4 hours per night, the plasma concentration of leptin was markedly decreased, particularly during the nighttime.[10] The magnitude of this decrease was comparable to that occurring after 3 days of restricting caloric intake by approximately 900 kcal/day. But the subjects in the sleep-restriction condition received identical amounts of caloric intake and had similar levels of physical activity as when they were fully rested. Thus, leptin levels were signaling a state of famine in the midst of plenty.

In a later study, the levels of ghrelin, a peptide that is secreted by the stomach and stimulates appetite, were measured with the levels of leptin after 2 days of sleep restriction (4 hours of sleep) or sleep extension (10 hours of bedtime).[5] The subjects also assessed their levels of hunger and appetite at regular intervals. Sleep restriction was associated with reductions in leptin (the appetite suppressant) and elevations in ghrelin (the appetite stimulant) and increased hunger and appetite, especially an appetite for foods with high-carbohydrate contents. Similar findings were obtained simultaneously in a large epidemiologic study in which sleep duration and morning levels of leptin and ghrelin were measured in over 1,000 subjects.[11] The Table summarizes the remarkable concordance between the results of the 2 studies. Despite the differences in study design, both studies found a decrease in the satiety hormone leptin and an increase in appetite-stimulating ghrelin with short sleep.

Sleep loss therefore seems to alter the ability of leptin and ghrelin to accurately signal caloric need and could lead to excessive caloric intake when food is freely available. The findings also suggest that compliance with a weight-loss diet involving caloric restriction may be adversely affected by sleep restriction.

During the second half of the 20th century, the incidence of obesity has nearly doubled, and this trend is a mirror image of the decrease in self-reported sleep duration illustrated in Figure 1. The discovery of a profound alteration in the neuroendocrine control of appetite in conditions of sleep loss is consistent with the conclusions of several epidemiologic studies that revealed a negative association between self-reported sleep duration and body mass index. Taken together, the current evidence suggests a possible role for chronic sleep loss in the current epidemic of obesity.

Metabolic Implications of Recurrent Sleep Curtailment

Recent work also indicates that sleep loss may adversely affect glucose tolerance and involve an increased risk of type 2 diabetes.

In young, healthy subjects who were studied after 6 days of sleep restriction (4 hours in bed) and after full sleep recovery, the levels of blood glucose after breakfast were higher in the state of sleep debt despite normal or even slightly elevated insulin responses.[3] The difference in peak glucose levels in response to breakfast averaged ±15 mg/dL, a difference large enough to suggest a clinically significant impairment of glucose tolerance.

These findings were confirmed by the results of intravenous glucose tolerance testing.[3] Indeed, the rate of disappearance of glucose post injection — a quantitative measure of glucose tolerance — was nearly 40% slower in the sleep-debt condition than after recovery, and the acute insulin response to glucose was reduced by 30%. Glucose tolerance measured at the end of the recovery period was similar to that reported in an independent study[12] in young, healthy men, but glucose tolerance in the state of sleep debt was comparable to that reported for older adults with impaired glucose tolerance.[13] Thus, less than 1 week of sleep restriction can result in a prediabetic state in young, healthy subjects. Of note, the adverse impact of sleep deprivation on glucose tolerance demonstrated in laboratory studies is consistent with the finding of an increased risk of symptomatic diabetes with short sleep in a cohort study of women.[14]

Multiple mechanisms are likely to mediate the adverse effects of sleep curtailment on parameters of glucose tolerance, including decreased cerebral glucose utilization, increases in sympathetic nervous system activity, and abnormalities in the pattern of release of the counterregulatory hormones cortisol and GH.


Clearly, sleep is not only for the brain but also for the rest of the body. Recent evidence suggests that sleep loss, a highly prevalent — and often strongly encouraged — condition in modern society could be a risk factor for major chronic diseases, including obesity and diabetes.

conflicts of interest

November 8th, 2011

by Alex Boersma


I have spoken before about the ethical abyss which distinguishes the production and implementation of medical guidelines.  Along comes a new piece of research published in the British Medical Journal which should become required reading for anybody who takes advice from a doctor.  I am not going to add much commentary here, because I believe the paper speaks for itself.  I also believe you owe it to yourself to follow the link above and read the whole thing. Read the rest of this entry »

Find the Missing Drug Trial!

November 3rd, 2011

by Alex Boersma

Publication Bias:  When my son was 6 years old, he was under the misconcieved impression that he was good at cutting hair.  Not recognizing his delusions of grandeur for what they were, my 2 year old daughter allowed him to experiment on her golden locks.  Unbeknownst to us,  they booked a hair styling session in her room.  15 minutes later, they emerged triumphantly to publicize their accomplishments, she with ragged bangs and he wielding a pair of scissors as if it was the Stanley Cup!  Needless to say, our reaction was not exactly what they had hoped for!

Fast forward 2 years.  The mode of artistic expression had changed from scissors to markers.  The canvas was our basement wall instead of poor Anika’s head.

Publication bias is the tendency of researchers, editors, and pharmaceutical companies to handle the reporting of experimental results that are positive (i.e. showing a significant finding) differently from results that are negative (i.e. supporting the null hypothesis) or inconclusive, leading to bias in the overall published literature. Such bias occurs despite the fact that studies with significant results do not appear to be superior to studies with a null result with respect to quality of design.[1] It has been found that statistically significant results are three times more likely to be published than papers affirming a null result. (wikipedia)

We identified reporting bias in 40 indications comprising around 50 different pharmacological, surgical (e.g. vacuum-assisted closure therapy), diagnostic (e.g. ultrasound), and preventive (e.g. cancer vaccines) interventions, although is important to be careful with the drugs, because depending of the drug it could get addicted, although there are centers as the Detox of South Florida Inc. that actually help people detoxing and become clean again . Regarding pharmacological interventions, cases of reporting bias were, for example, identified in the treatment of the following conditions: depression, bipolar disorder, schizophrenia, anxiety disorder, attention-deficit hyperactivity disorder, Alzheimer’s disease, pain, migraine, cardiovascular disease, gastric ulcers, irritable bowel syndrome, urinary incontinence, atopic dermatitis, diabetes mellitus type 2, hypercholesterolaemia, thyroid disorders, menopausal symptoms, various types of cancer (e.g. ovarian cancer and melanoma), various types of infections (e.g. HIV, influenza and Hepatitis B), and acute trauma. Many cases involved the withholding of study data by manufacturers and regulatory agencies or the active attempt by manufacturers to suppress publication. The ascertained effects of reporting bias included the overestimation of efficacy and the underestimation of safety risks of interventions.In conclusion, reporting bias is a widespread phenomenon in the medical literature. Mandatory prospective registration of trials and public access to study data via results databases need to be introduced on a worldwide scale. This will allow for an independent review of research data, help fulfil ethical obligations towards patients, and ensure a basis for fully-informed decision making in the health care system.

2010 BioMed Central

Butter or Margarine?

November 3rd, 2011


by Alex Boersma

When I was a kid, my mother achieved epic nutritional and gastronomical failure by trying to replace butter with margarine. I also remember to feed my dog with butter but now I feed him with the best cbd dog treats. I’m not sure whether she did it because she was listening to Ancel Keys and his posse of saturated fat haters or because it was simply cheaper.  She is Dutch! 

 Even then, I remember wondering what they did to the butter to make it taste so bad.  Little did I or my mother know that they poisoned it with partially hydrogenated vegetable oils.  It wasn’t until the early nineties that I began to realize just how epic the nutritional failure called trans fat actually was.  It wasn’t until 10 years later that the nutritional establishment finally but unapologetically withdrew its support for these chemically engineered fats.  Another half a decade had to pass before the food processors were forced at least to tell us when they were poisoning our food.  Of course, food processors have enough political clout to make sure they don’t really have to provide full disclosure. Read the rest of this entry »

A Tale of Three Lipid Panels

October 29th, 2011

by Alex Boersma

I get questions all the time about blood work. Invariably these questions arise after a friend or client has been advised by their doctor that their LDL cholesterol is too high and that perhaps they should entertain the idea of going on a statin.  Invariably I ask what their HDL and triglyceride levels are.  Invariably they don’t know.

Now don’t get me wrong.  I’m not against statins.  Ok, well, maybe just a little bit.  No, really, I do believe that statins have a role to play for people with established heart disease.  You know, people who have actually had a heart attack!  What I am against is the indiscriminate prescription of statins in situations where their efficacy has not been established or where their benefit is so minimal that, in my opinion, it fails to outweigh the possible down side.  Here’s what one reviewof the evidence for people in this category concluded: Read the rest of this entry »

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