Functional Health Services for Your Well Being

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 »

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 »

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 »

Diabetes Part II

October 5th, 2011

by Alex Boersma

In part I of this series, I identified Type II diabetes as the most pernicious and calamitous disease of the 21st Century, responsible for destroying the health of millions of Canadians and bankrupting our health care system.  I established that this destructive epidemic is characterized primarily by the inability to regulate blood sugar and is precipitated by a metabolic dysfunction called insulin resistance. 
It is clear that if we expect to mitigate the consequences – both personal and social – of this 21st century epidemic called DIABETES, we must begin with a thorough understanding of all that is known about insulin resistance.  Despite a profusion of misconceptions, the research on insulin resistance is fairly consistent in it’s conclusions.
Sorry, high blood sugar and/or insulin are not up there!  Read the rest of this entry »

China Study Revisited

September 2nd, 2011

About 10 months ago I wrote an article entitled The China Study – How Not to do Science.  I wrote it with the express intention of  having a resource to which I could direct people who questioned me about the value of Colin Campbell’s ode to veganism.  Unfortunately, my design to make things easier on myself hasn’t worked out quite the way I had expected.  Instead of having to explain myself less, I find myself continually entangled in lengthy disourses supporting my position.  It seems I have decidedly underestimated the emotional and intellectual investment most people have already made in Campbell’s hyperbole by the time they ask me about the book.  Either that or I’m just wrong about all this! Read the rest of this entry »

More Justifaction of Statins

May 21st, 2011

by Alex Boersma

JUPITER: Best CVD event reduction in patients with very low LDL-cholesterol levels

Heartwire – April 15, 2011

The JUPITER study:  Justification for the Use of Statins in Primary Prevention.  The name says it all.  This study was designed to justify the use of statins for people who do not have heart disease.  In other words:

We think lots of people should take statins, regardless of whether or not they have heart disease.  Let’s design a study which will justify millions of new clients for our expensive new drug!



Purveyors of pharmaceutical grade justification  Read the rest of this entry »

Diabetes – Part I

April 10th, 2011

by Alex Boersma

From the Canadian Diabetes Association:

Today, more than 9 million Canadians live with diabetes or prediabetes – a condition that, if left unchecked, puts you at risk of developing type 2 diabetes.  This means that nearly 1 in 4 Canadians either has diabetes or prediabetes.  More than 20 people are diagnosed with the disease every hour of every day.

The serious complications
Diabetes can lead to serious complications and premature death:

  • 80% of Canadians with diabetes die from a heart attack or a stroke;
  • 42% of new kidney dialysis patients in 2004 had diabetes.
  • Diabetes is the single leading cause of blindness in Canada;
  • 7 of 10 non-traumatic limb amputations are the result of diabetes complications;
  • 25% of people with diabetes suffer from depression;
  • The life expectancy for people with type 1 diabetes may be shortened by as much as 15 years; and
  • The life expectancy for people with type 2 diabetes may be shortened by 5 to 10 years.

The cost of diabetes in Canada
Not only is diabetes a personal crisis for people with the disease, it is also a tremendous financial burden for the Canadian healthcare system and society as a whole.  The cost of diabetes for 2010 is approximately $12.2 billion, which is nearly double its level in 2000.  The cost of the disease is expected to rise to $16.9 billion by 2020. Now the country is doing the best possible to allow the use of  CBD UK oils to treat diabetes, it has shown a highly improvement regarding appetite, energy balance and insulin sensitive among others, plus CBD oils can be easier to afford than other treatments.    

Type II Diabetes Mellitus (T2DM) is unquestionably the most pernicious and calamitous disease of the 21st century.  The underlying dysregulation of blood sugar is devastating to both our health and our health care system.  If we are unable to control blood sugar, we will remain impotent in the battle against obesity, heart disease, or probably even cancer.  Oh, and don’t forget blindness, kidney disease, fatty liver disease and depression!  The cost to our vitality as we age will be monumental.  To our health care system, it will be disastrous.

How best to control this emerging epidemic is the subject of considerable debate.  On the one hand, national health institutions such as the Canadian Diabetes Association contend that this is a disease governed by abnormal fat regulation.  These institutions declare that a change in dietary fat consumption is the key to regulating blood sugar, and that carbohydrate consumption is only a minor part of the problem.  On the other hand, there are numerous established clinicians like Drs.  Mary Vernon and Richard Bernstein, who have had great success in controlling and even reversing diabetes by rigorously curtailing carbohydrate consumption and enthusiastically endorsing a high fat diet. Read the rest of this entry »

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