With the recent discussion of water intake and health- here is an excerpt from The Original Prescription that discusses the principle of using water as our main source of hydration and a little bit about the origins of the 8 glasses per day “rule.”

This is just one of over 50 Lifestyle principles discussed in the Original Prescription.

Principle #6: Water should be your primary beverage; drink enough, and try to limit the number of liquid calories you consume.

Water is one of the quintessential nutrients of life and yet is often one of the most commonly neglected. Despite its great importance for nearly every bodily function, many of us are still at a loss when it comes to knowing how much we’re supposed to drink each day and which other beverages count toward our daily needs. All this confusion about water needs comes as no surprise considering that the first official recommendation for adequate intake (AI) of water was only established in 2004 by the Institute of Medicine, coinciding with an increase in popular awareness about water needs for preventing conditions such as cancer, heart disease, and weight gain (27). Prior to that, the RDA concluded that it was impossible to set a recommendation for water needs, and the National Research Council used a general rule of thumb of 1 ml/ kcal (that would be two liters of water per 2000 calories consumed, if you’re getting out your calculator) (28). Today’s recommendations for daily water requirements, however, are based on national averages from the NHANES III data, although individual needs vary greatly. It’s estimated that most of us need to get 80% of our daily hydration through beverages, mostly water, while about 20% of our hydration comes from the food we eat (less if you happen to avoid fresh fruits and vegetables) (28).

Throughout history, humans have relied on water as their primary source of hydration, struggling to ensure both an abundant and a clear source was available for their survival. Unfortunately, this struggle still exists in many locations around the world today. In the West, water abundance (at least for drinking) is rarely in jeopardy, and yet many choose other options. Countless individuals have replaced water with soft drinks to quench their thirst, and, as a result, sweetened beverages have become one of the major sources of calories in the American diet. Consumption of high fructose corn syrup, the major sweetener in commercial soft drinks, increased over 1000% between 1970 and 1990, and today, half of all Americans consume soft drinks every day. In fact, these beverages now constitute the leading source of added sugar in the average diet (29,30). To make matters worse, the calories provided by soft drinks often fail to satisfy hunger the way solid food does, nor do they quench our thirst in the way water can, making sugary beverages a key player in the obesity epidemic (30–33). If you want to maintain those good signals that your body is waiting for, limit the number of calories you consume through drinks. So how much water should you drink per day?  Well, that depends. How much you weigh (roughly 60% of that is water), how much water you lost recently to perspiration, and relative humidity will all affect the ultimate answer. The Institute of Medicine says that the adequate intake of total water per day is 3.7 liters for men and 2.7 liters for women.† The “8 by 8 rule” (8 glasses of 8 oz. each) equates to about 2 liters. Many rely on their thirst to tell them when to drink, and while it is true that most people’s thirst and hunger mechanisms can help manage their net water balance, in many people the thirst mechanism is blunted and mild dehydration can set in well before their body tells them to drink. Others try to rely on the color and darkness of their urine as a gauge of hydration, but this is not always a reliable indicator of the need for water (35)

So what’s the bottom line when it comes to hydration and water?

  • If you aren’t already doing it, drink mostly water to keep yourself hydrated.
  • Make sure your water source is clean and free of contaminants.
  • Tea and coffee are fine for most people (in moderation); if the caffeine causes you to urinate frequently, consider offsetting this loss with additional water.
  • Alcohol is dehydrating—plain and simple.
  • Remember to include water-based soups and stews, herbal teas, and low-sugar fruit juices.
  • Drink more water when you are physically active and when the weather turns hotter.

† The AIs provided are for total water in temperate climates. All sources (according to IOM) can contribute to total water needs: beverages (including tea, coffee, juices, sodas, and drinking water) and moisture found in foods. Moisture in food accounts for about 20% of total water intake.

Get your copy of The Original Prescription on our Website or on Amazon.

I was recently reminded of how impressive berberine can be after recently hearing a clinician’s story. The particular patient had Type 2 diabetes and this clinician had been treating him for 15 years. Consistently his glycated hemoglobin was above 9% (aim: to be below 7%). Historically, the patient had been taking 2 grams of Metformin, then recently these meds were lowered to 1 g and berberine was added. Within one month, his glycated hemoglobin was 6.7%. Obviously, this is a single case and other factors may have been involved- lthough the clinician was convinced berberine was a major factor in these results.

We have been following the growing research related to use of the alkaloid compound berberine for almost a decade now and wanted to give a short update for those interested in using this dietary supplement as part of their healthcare protocol for managing glucose, lipids or related cardiovascular outcomes.

Berberine for glucose management in Type 2 Diabetes

Most of the excitement related to the use of berberine for diabetic patients comes from a paper published in early 2010 (Metabolism 59(20)) where a group of Type 2 diabetic patients were given either metformin 1.5 g/d (n=26), rosiglitazone 4 mg/d (n=21) or berberine HCl 1g/day (n=-50) and followed for 2 months. The remarkable results showed drops in fasting blood glucose and glycated hemoglobin for berberine which matched both metformin and rosiglitazone- while only the berberine group saw a statistical drop in TG levels. Furthermore, they followed this study by testing 1g/day of berberine HCl in type 2 diabetic patients who had either hepatitis B or C to detect whether these same outcomes could be confirmed in these patients and what affect berberine may have on liver enzymes in these patients. They found similar benefits in both blood glucose and TG levels as in the non-hepatitis patients, but also a statistical improvement in both AST and ALT enzyme levels.

One of the critiques of this (and most) berberine studies is that they have nearly all been performed in China- on Chinese subjects and most of the published trials are in Chinese- making the data difficult to assess and translate (both linguistically and clinically) into practice here in the US. A recent meta-analysis of these Chinese studies has recently been published (in English) and is available for download online (Evidence-Based Complementary and Alternative Medicine Volume 2012). While showing a consistent positive benefit for berberine in a wide-range of Chinese subjects (14 trials, 1068 subjects), the authors also conclude that many of these trials were poorly conducted and the need for a large, well-controlled and randomized clinical trial is critical. Nonetheless, they found berberine generally safe- listing GI discomfort and constipation (berberine is traditionally used to treat diarrhea in China) as side-effects to treatment in a small number of patients.

Berberine for lipid-altering effects or related cardiovascular outcomes

Years before the glucose-related outcomes were being published, researchers in China had described lipid-altering effects using berberine. Some of these trials are now being performed outside of China in Caucasian subjects. Most recently was a study done at the University of Pavia (Italy) in 144 subjects with low cardiovascular risk (Expert Opin Biol Ther 2013). After a 6-month run-in period of diet and physical activity, patients were randomly given either placebo or berberine (500 mg- twice per day) for 3 months. Patients were taken off their experimental therapy for 2 months (wash-out), and then placed back on berberine or placebo for an additional 3 months. Not only was berberine deemed safe in these individuals, but subjects consuming berberine had reduced total cholesterol, LDL-cholesterol and TG, and increased HDL-cholesterol. All of these benefits were diminished during the washout period but returned once back on berberine.

A small pilot study, done also in Caucasian subjects, was performed here in the US (U. of South Dakota and South Dakota State University) which explored the lipid-lowering effect of berberine (Phytomedicine 2012). Sixteen obese subjects were given berberine (500 mg- 3 times per day) for 12 weeks. As a pilot study, there was no control group. After 12 weeks they saw a modest loss in body weight (avg. 5 lbs/subject) and a significant reduction in total cholesterol (-12.2%) and triglyceride levels (-23%). 2 subjects stopped the protocol due to GI complaints- which may have been due to the higher dose (1.5 grams) over other studies using only 1 gram.

A review and meta-analysis of the Chinese studies looking at the lipid altering effects of berberine is also online (Planta Medica Abstract-2013)

Other Recent Human Studies using berberine

Potential for berberine/drug interactions

“CONCLUSIONS: Repeated administration of berberine (300 mg, t.i.d., p.o.) decreased CYP2D6, 2C9, and CYP3A4 activities. Drug-drug interactions should be considered when berberine is administered.”

Animal or Mechanism studies of interest

One of the most impressive aspects of the recent berberine studies is the vast number of animal, tissue and mechanistic studies which have been emerging in the past few years. Listed below is just a few recent studies related to metabolic pathways and outcomes. I will only highlight one particular study because it is a fascinating relationship between a nutraceutical agent, the gut microbiome and human physiology.

One of the main historical uses for berberine (Coptis chinensis and its extracts) within Traditional Chinese Medicine is for intestinal infections and diarrhea. This has led some to wonder if consuming berberine regularly for cardiometabolic outcomes might promote an imbalance within the gut bacteria (microflora). As it turns out, the answer might be yes, but in a very helpful way. In a study published in PLoS ONE (Full Article Free online), researchers show that the prevention of obesity and insulin resistance which occurs in rats fed a high-fat diet are partially mediated by changes to the gut microflora. This mechanism adds to the long list of known metabolic influences that berberine has on metabolic pathways and links to the growing evidence we now have of the relationship between obesity and gut microflora in humans. While the paper is quite technical, it gives some interesting background information and highlights the type of research that will continue to be done to decipher the benefits of berberine and other nutraceutical agents. It also shows us that some agents have activities which don’t even require absorption to result in a clinical outcome.

Here are more studies on berberine that might interest you:






In the past weeks, two important papers have been published which were intended to advance the understanding of the role of carnitine in human health (or disease). The one, which appears to suggest carnitine is potentially harmful, you might already know about; the other, which shows the repeated benefit of carnitine, you may not have heard about (yet). We will attempt to synthesize the information in these two papers (along with some background information) to see if we can come to a reasonable understanding of the role of carnitine as a dietary supplement. A brief “Final Point” can be found at the end.

First of all, for those less familiar with carnitine; it is an amino acid-like compound which our bodies can synthesize from the amino acids lysine and methionine. Natural sources of carnitine come primarily from red meat and dairy, although lesser amounts can be found in a variety of foods such as fish, nuts, tempeh and avocados.  Its main biological function is to help transport acyl-groups from fatty acids into mitochondria where they can be used as energy for the cell (via beta-oxidation).  As a dietary supplement, L-carnitine has been used primarily for heart conditions, male fertility, sperm health, weight loss and energy.

The first paper we will discuss was published in Nature Medicine from the prestigious group at the Cleveland Clinic. This was an ambitious project and paper- covering a wide range of experiments in both human and animal subjects. The title itself is a bit provocative: “Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis”, immediately tying this research with red meat consumption and risk for heart disease. Needless to say it has set off a number of debates- some of which I will point you to throughout the rest of this brief discussion.

What they reported was essentially that certain bacteria in our gut can convert carnitine (and other compounds) into a molecule called TMA (trimethylamine), which can be further converted by our liver to TMAO (trimethylamine oxide). TMAO has been shown in other studies to increase the risk for atherosclerosis. Further, they found that in vegetarians (at least those they tested) conversion of carnitine (from beef or supplements) was not converted to TMA because the bacteria required for the conversion are not abundant enough to allow for this conversion. No TMA- no conversion to TMAO- and therefore a reduced atherosclerotic risk (-or so the logic is assumed). They also showed that in a large number of patients coming in for voluntary cardiac evaluation- those with the highest levels of blood carnitine had a higher calculated risk for certain cardiovascular events. The researchers also conducted several studies in mice which were fed carnitine and they found consistent changes in the gut microbiota- allowing for selectively more carnitine to TMA conversion.

The paper, at first, seems to be airtight and quite convincing; until you really begin to look at the details of each experiment and the broader question of the role of TMAO in the diet. Since there is an extremely detailed discussion of these issues and critiques of this paper at the Weston Price Foundation Website online (not for the scientific faint of heart), I will just give you the gist of it here.

  • To focus on “red meat” and carnitine in particular as notable substrates for the generation of TMAO in humans is odd when previous studies have shown that serum TMAO is much higher in subjects after the consumption of numerous vegetable and greatly increased (up to 100X) when consuming certain types of seafood. The authors even say “An analyte with identical molecular weight and retention time to L-carnitine was not in the top tier of analytes that met the stringent P value cutoff for association with CVD. However, a hypothesis-driven examination of the data using less stringent criteria (no adjustment for multiple testing) revealed an analyte with the appropriate molecular weight and retention time for L-carnitine that was associated with cardiovascular event risk (P=0.04).”[emphasis added] One might ask why their hypothesis-driven examination focused on a relatively low TMAO inducing agent with no association with CVD which happens to be in red meat.
  • Much of the data between vegetarian and omnivore subjects were dependent on few, and in some cases, single individuals. Apparently convincing vegetarians to consume meat was more challenging than they initially figured. Some of this data is, at best, hypothesis generating- but is far from conclusive. These issues are further complicated since the gender of the vegetarian and the omnivore were different and there is known sex-based differences in the enzyme activities which form TMAO in humans. Since diet is very important to the formation of the human gut bacteria environment, I don’t doubt there may be significant differences in the microbiota between vegetarians and omnivores/carnivores- even in their ability to convert carnitine into TMA. It may also be that other beneficial compounds made by these same organisms would be absent or diminished in vegetarians- limiting other benefits derived from carnitine.
  • The mouse studies, again, are very interesting and should be the basis of future studies but the ability to translate these results to humans is very tenuous at best. By anyone’s calculations, the amount of carnitine given to these mice greatly exceeds the doses which could be consumed by humans eating meat or by supplementation. Likewise, the changes in microbiota in mice which resulted from carnitine consumption is difficult to contextualize since as the authors tell us “Notably, a direct comparison of taxa associated with plasma TMAO concentrations in humans versus in mice failed to identify common taxa. These results are consistent with prior reports that microbes identified from the distal gut of the mouse represent genera that are typically not detected in humans” I am guessing we will see follow-up studies in humans.
  • Finally, the authors report two relationships between blood carnitine levels and risk for cardiovascular disease. In one data set- they report that the predicted risk is higher at the highest blood level of carnitine; however when they actually correlated fasting carnitine levels with known major adverse cardiac events over a 3-year period (adjusted for comorbidities and traditional risk factors) there was no increased incidence of events (see discussion on Mayo Clinic paper below).

Again- further details on these and other finer points can be found at the Weston Price Foundation’s online discussion of this paper for those interested. The Cleveland Clinic group has certainly illuminated us on the role of intestinal microbiota in the conversion of food substances and potential health outcomes (this is likely to be a huge area of future research on bioactives in food and supplement in the next decade) – but this data is not sufficient yet to demonstrate that red meat or the carnitine it delivers contributes to the risk of heart disease in humans.

Now, on to the second big carnitine paper from last week (the one you may not have heard about yet). This paper was published in the Mayo Clinic Proceedings and is a systematic review and meta-analysis of a number of clinical trials published since the mid-1980’s using L-carnitine as a supplement. Specifically, since myocardial carnitine levels are quickly diminished during ischemic events (like an MI), they looked at only those studies which used L-carnitine supplements (compared to placebo) in individuals with a previous acute myocardial infarction (AMI). The studies that met their criteria looked at outcomes like all-cause mortality, ventricular arrhythmias, myocardial reinfarction, heart failure or angina. In all, 13 studies met there criteria for evaluation which included 3629 patients. In their statistical analysis, L-carnitine consumption was associated with a 27% reduction in all-cause mortality, a 65% reduction in ventricular arrhythmias, and a 40% reduction in angina symptoms compared to placebo in these post-AMI patients. A non-statistical trend toward reduced risk was seen with both heart failure and myocardial reinfarction.

As anyone who has reviewed meta-analysis data can tell you, these types of analysis are far from definitive evidence for (or against) a particular therapy. Different doses were used, different routes of administration and slightly different outcomes measured always makes the pooling of data from experiments performed over several decades for statistical analysis less than perfect; this study is no exception. Also, like many other dietary supplement trials-many of those selected for this meta-analysis were small trials.

Individually, while many of these studies did not reach statistical significance for some of the outcome measurements, in nearly every case, the benefit clearly favored carnitine over the placebo. Pooling the data increases the statistical significance, but it did not change the clear benefit from these studies. In fact, only one measurement in a single study (a 1995 study looking at reinfarction) showed a benefit for the placebo group (albeit non-statistical) which was enough to prevent the overall benefit in the pooled data for this measurement.

As always they suggest (and we agree) that more studies (larger, better) be performed to assess the role of L-carnitine as a supplement for post-AMI patients (and other cardiovascular outcomes). What we can say from these data is there appears to be no harm in using L-carnitine in patients for secondary prevention of cardiovascular disease- and a strong likelihood of benefit. Certainly, future studies will likely address TMAO production in light of the Cleveland Clinic study above. It may be possible to discover a relationship between certain intestinal microbiota which enhance or diminish the use of L-carnitine as a bioactive agent.

While I don’t have time to add more here- check these recent papers for more about the use of carnitine (as a supplement):

Final Point: Q&A

Q: Should we avoid or limit the use of L-carnitine in foods or supplements in order to avoid the potential risk for cardiovascular disease?

A: There is no evidence that avoiding carnitine will reduce CVD. If we are convinced that the formation of TMAO is a leading cause of atherosclerosis (I’m not yet), the conversion from carnitine to TMAO is a minor contributor even at extremely high supplemental (or dietary) levels; furthermore, individuals with cardiovascular disease appear (from the Mayo Clinic paper) to be protected from secondary events when using supplemental carnitine; a finding which shows that higher doses are more protective.

Q: Is Red Meat Bad for your health?

A: This is a much bigger topic than we can cover here and, of course, very controversial. Our position is that the majority of the risks associated with meat can be attributed to processed meat consumption, certain cooking methods for meat (frying, charring etc.) and the fact that many people who eat meat also have a wide-range of poor eating patterns (low fruit and vegetable consumption, low consumption of good fats, increased use of potatoes, breads and refined sugars etc.). Within the background of a prudent diet (like the Mediterranean diet), red meat, poultry and fish should not increase risk for chronic disease.

Q: Are there probiotics that can be taken which will reduce/eliminate the conversion of carnitine or other substances to TMA in our GI tract?

A: We don’t know yet. Certainly this type of research will be conducted in the future as the role of probiotics in a wide-range of health conditions are being explored. My guess is that we will, over the next decade or so, find specific blends of probiotics which may sufficiently modulate the GI microbiota to compensate for many disease-related conditions.

 [Image courtesy of piyato / FreeDigitalPhotos.net]

Your chances of death may depend on the county you live in, according to a new National Survey, but the reasons for the startling findings boil down to lifestyle factors. Healthy eating habits, smoking, and the environment, including quality of local parks and water were all key components of the ratings. Some of the worst scoring counties in the Survey included: Lake in CA, New Haven in CT, Baltimore City in MD and Menominee in WI – check out the article to see how your county scored!


Losing weight is always difficult, but what if extra fat may be the body’s only defense from dangerous fat-soluble toxins?  Remember the adage: “The solution to pollution is dilution”- we attempt to dilute poisons to reduce their concentration and therefore, their toxic effects. In the case of fat-soluble toxins, many compounds actually trigger the body to produce fat as a protective storage for these additional toxins. This keeps the toxins away from sensitive tissues and cells, but increases body fat and weight which can lead to other serious concerns.

Two things you should think about if you are a clinician or a patient. If you are attempting to lose a lot of weight quickly and you have never considered a detoxification program you should be aware that massive fat reduction will put additional strain on the liver and gall bladder as additional toxins will be released from fat stores and moved into the liver and other tissue. The toxins will also be working to tell your body to produce more fat to re-dilute the toxins. Losing weight slowly while changing the diet to include helpful liver cleansing foods is much healthier. Consider doing a medically appropriate detoxification program after you have lost 10-15 lbs to blunt this affect. Or, consider doing a detoxification program as the start to your weight-loss program.

Below are some links to recent papers which shows the links of certain toxins to obesity and weight-loss- and several showing how pollutants increase risk for diabetes. Some food for thought for the New Year.

November is Diabetes Awareness Month and there are some interesting facts you might want to be aware of. According to the latest data released by the CDC, diabetes rates have been increasing at an alarming rate over the past two decades; but not to worry; over 200 new drugs are currently in the pipeline to save us. If you didn’t detect my sarcasm, let me be clear: these two ”unrelated” pieces of information show that we still have much more to be aware of before we can make any headway in our current diabetes crisis.

The CDC released data this month that shows that the number of diagnosed cases of diabetes between 1995 and 2010 grew by 50% or more in 42 states (in the US), and by 100% or more in 18 states. States with the largest increases over the 16-year period were Oklahoma, up 226%; Kentucky, up 158%; Georgia, up 145%; Alabama, up 140%, Washington, up 135%, and West Virginia, up 131%.

And our “hope” to slow this colossal devastation of our health and healthcare system? More drugs, of course. According to the Pharmaceutical Research and Manufacturers of America (PhRMA) there are no less than 221 drugs in clinical trials or in the process of FDA approval for diabetes (Type 1, type 2, or diabetes complications) [See News Report here]. Billions of dollars will be spent so a few of these can make it to market; and if I can make a prediction, 10 years from now the diabetes rates will continue to increase and many of these drugs will have been approved and recalled by FDA due to their sides effects. (I can’t help from thinking that the rampant use of statin drugs in the past decade has played a significant role in driving the diabetes numbers in the previous story- but I digress)

While it is agreed upon by most researchers that 70-80% of the cases of diabetes (Type 2) are preventable with lifestyle prevention/intervention; the vast majority of research dollars are still spent on finding solutions which avoid this solution! This is the type of “awareness” that is desperately needed if we are truly to reverse this, and most of the chronic diseases that are plaguing us today- and also the reason I wrote the Original Prescription in the first place. Our solutions must address the root cause if we hope to change the numbers the CDC reports a decade from now.

I wanted to let you know about the St. Louis Institute for Integrative Medicine 3rd annual Symposium last weekend (www.sliim.org). The meeting was held on the campus of Missouri Baptist University in Chesterfield. This conference is unique in that it includes both clinicians and their patients (and potential patients), a great model for other communities to emulate.

I opened the conference with a talk called “Your DNA is not your Destiny: How to Trump Your Genetics With Healthy Choices”- allowing me to highlight many of the concepts I developed in The Original Prescription. I was joined by a great faculty of speakers, including Jill Carnahan M.D., Bryan Warner M.D., and Carrie Carda, MD; as well as a host of great vendors from the local community. It reminded me of how many times I have run into clinicians over the years who had no local community of like-minded clinicians to encourage them and bounce ideas off of. It is important to understand that the power of community is not just a benefit to the patient, it is a must for a healthy clinician and medical practice as well. For me it was encouraging to see some long-time friends and meet so many new ones. I would also like to mention Ortho Molecular’s local representative, Kristen Brokaw- her skills and vision are one of the reasons SLIIM exists in the first place. The future of functional and integrative medicine needs more events like SLIIM all over the country…and the world.

(photos coming soon!)


(Preface of The Original Prescription)
Those who know me are well aware that I have spent over 16 years researching and developing evidence-based nutritional supplements (nutraceuticals) for use by clinicians and their patients. You might think it curious, then, that the first manuscript I decided to expand into a book is about lifestyle medicine. The reason is simple. I firmly believe that every therapy, including nutritional supplementation, must be rooted in the fundamental signaling pathways designed to keep us healthy. Those signals and that design are what this book is all about. In many ways, I have been thinking about some of these ideas since my graduate school days, studying molecular immunology and debating the meaning of life with my fellow students. When you really begin to understand the elegant processes that drive the functions we call “life,” you will just shake your head in amazement. My hope is that in my description of the simple complexity that converts our lifestyle decisions into health, you will first be amazed and then inspired to leverage these ideas to pursue your own optimal health. The fundamental principles we outline here are not “new” per se; they are, after all, The Original Prescription. What is new is that our understanding of how and why these interventions work has been expanded with recent scientific research; and when we understand how something works, we are able to leverage its benefits. In this case, understanding the mechanisms behind lifestyle signals allows you to create a synergistic effect using multiple lifestyle intervention strategies. Knowing how these interventions work will also allow you to modify them to fit your unique health history and circumstance, and, because these concepts are fundamental principles, they won’t become useless once the next health fad or research paper comes and goes. As an aside, my other great pursuit is the study of biblical history, language, culture and influence. I have included a few brief anecdotes from these pursuits, mostly in the form of footnotes, for your consideration as well. It would have been easy in a book like this to point the finger of blame toward all those who have contributed to the poor lifestyles driving our healthcare crisis. The usual suspects of agribusiness, Big Pharma, insurance companies, fast-food chains, government regulation, FDA, poor parenting, and the like are easy targets. The fact is there is plenty of blame to be shared by all. Ultimately, most of the decisions that affect your health are yours to make. The principles outlined in this book have a powerful potential to turn your health around but are impotent if left neglected and untried. My hope is that you will, instead, choose to fulfill The Original Prescription.
– Dr. Thomas Guilliams