Dr. Zimmerman's New Info/Perspective on Vaccines Posted on March 14, 2019, 0 Comments

American Association of Physicians and Surgeons Denounce Mandatory Vaccination Posted on March 07, 2019, 0 Comments

Original Source found here: https://aapsonline.org/measles-outbreak-and-federal-vaccine-mandates/

To:  Oversight and Investigations Subcommittee, House Energy and Commerce Committee

Senate Committee on Health, Education, Labor and Pensions

Re: Statement federal vaccine mandates

Feb. 26, 2019

The Association of American Physicians and Surgeons (AAPS) strongly opposes federal interference in medical decisions, including mandated vaccines. After being fully informed of the risks and benefits of a medical procedure, patients have the right to reject or accept that procedure. The regulation of medical practice is a state function, not a federal one. Governmental preemption of patients’ or parents’ decisions about accepting drugs or other medical interventions is a serious intrusion into individual liberty, autonomy, and parental decisions about child-rearing.

A public health threat is the rationale for the policy on mandatory vaccines. But how much of a threat is required to justify forcing people to accept government-imposed risks? Regulators may intervene to protect the public against a one-in-one million risk of a threat such as cancer from an involuntary exposure to a toxin, or-one-in 100,000 risk from a voluntary (e.g. occupational) exposure. What is the risk of death, cancer, or crippling complication from a vaccine? There are no rigorous safety studies of sufficient power to rule out a much higher risk of complications, even one in 10,000, for vaccines. Such studies would require an adequate number of subjects, a long duration (years, not days), an unvaccinated control group (“placebo” must be truly inactive such as saline, not the adjuvant or everything-but-the-intended-antigen), and consideration of all adverse health events (including neurodevelopment disorders).

Vaccines are necessarily risky, as recognized by the U.S. Supreme Court and by Congress. The Vaccine Injury Compensation Program has paid some $4 billion in damages, and high hurdles must be surmounted to collect compensation. The damage may be so devastating that most people would prefer restored function to a multimillion-dollar damage award.

The smallpox vaccine is so dangerous that you can’t get it now, despite the weaponization of smallpox. Rabies vaccine is given only after a suspected exposure or to high-risk persons such as veterinarians. The whole-cell pertussis vaccine was withdrawn from the U.S. market, a decade later than from the Japanese market, because of reports of severe permanent brain damage. The acellular vaccine that replaced it is evidently safer, though somewhat less effective.

The risk: benefit ratio varies with the frequency and severity of disease, vaccine safety, and individual patient factors. These must be evaluated by patient and physician, not imposed by a government agency.

Measles is the much-publicized threat used to push for mandates, and is probably the worst threat among the vaccine-preventable illnesses because it is so highly contagious. There are occasional outbreaks, generally starting with an infected individual coming from somewhere outside the U.S. The majority, but by no means all the people who catch the measles have not been vaccinated. Almost all make a full recovery, with robust, life-long immunity. The last measles death in the U.S. occurred in 2015, according to the Centers for Disease Control and Prevention (CDC). Are potential measles complications including death in persons who cannot be vaccinated due to immune deficiency a  justification for revoking the rights of all Americans and establishing a precedent for still greater restrictions on our right to give—or withhold—consent to medical interventions? Clearly not.

Many serious complications have followed MMR vaccination, and are listed in the manufacturers’ package insert, though a causal relationship may not have been proved. According to a 2012 report by the Cochrane Collaboration, “The design and reporting of safety outcomes in MMR vaccine studies, both pre- and post-marketing, are largely inadequate” (cited by the National Vaccine Information Center).

Mandate advocates often assert a need for a 95% immunization rate to achieve herd immunity. However, Mary Holland and Chase Zachary of NYU School of Law argue, in the Oregon Law Review, that because complete herd immunity and measles eradication are unachievable, the better goal is for herd effect and disease control. The best outcome would result, they argue, from informed consent, more open communication, and market-based approaches.             

Even disregarding adverse vaccine effects, the results of near-universal vaccination have not been completely positive. Measles, when it does occur, is four to five times worse than in pre-vaccination times, according to Lancet Infectious Diseases, because of the changed age distribution: more adults, whose vaccine-based immunity waned, and more infants, who no longer receive passive immunity from their naturally immune mother to protect them during their most vulnerable period.

Measles is a vexing problem, and more complete, forced vaccination will likely not solve it. Better public health measures—earlier detection, contact tracing, and isolation; a more effective, safer vaccine; or an effective treatment are all needed. Meanwhile, those who choose not to vaccinate now might do so in an outbreak, or they can be isolated. Immunosuppressed patients might choose isolation in any event because vaccinated people can also possibly transmit measles even if not sick themselves.

Issues that Congress must consider:

• Manufacturers are virtually immune from product liability, so the incentive to develop safer products is much diminished. Manufacturers may even refuse to make available a product believed to be safer, such as monovalent measles vaccine in preference to MMR (measles-mumps-rubella). Consumer refusal is the only incentive to do better.
• There are enormous conflicts of interest involving lucrative relationships with vaccine purveyors.
• Research into possible vaccine adverse effects is being quashed, as is dissent by professionals.
• There are many theoretical mechanisms for adverse effects from vaccines, especially in children with developing brains and immune systems. Note the devastating effects of Zika or rubella virus on developing humans, even though adults may have mild or asymptomatic infections. Many vaccines contain live viruses intended to cause a mild infection. Children’s brains are developing rapidly—any interference with the complex developmental symphony could be ruinous.
• Vaccines are neither 100% safe nor 100% effective. Nor are they the only available means to control the spread of disease.

AAPS believes that liberty rights are unalienable. Patients and parents have the right to refuse vaccination, although potentially contagious persons can be restricted in their movements (e.g. as with Ebola), as needed to protect others against a clear and present danger. Unvaccinated persons with no exposure to a disease and no evidence of a disease are not a clear or present danger.

AAPS represents thousands of physicians in all specialties nationwide. It was founded in 1943 to protect private medicine and the patient-physician relationship.

Respectfully yours,

Jane M. Orient, M.D., Executive Director
Association of American Physicians and Surgeons

US Health vs. other Countries Posted on February 25, 2019, 0 Comments

When US trends snowball, they often end up melting under their own momentum.

Original source found here:

https://ourworldindata.org/the-link-between-life-expectancy-and-health-spending-us-focus

Emotional Balance Posted on February 20, 2019, 0 Comments

Working on balance with a client this a.m. and he kept getting frustrated with how challenging it was for him. "I should do better," he kept chastising himself.

I tried to explain to him how his emotions were impacting his equilibrium. I used the analogy of walking across a balance beam. Put it 6 inches off the floor, and he'd likely have no problem. Now suspend the beam 100 feet off the ground, and fear will make that same walk seem a lot more precarious (and it is--but only because the mind has made it so).

Don't fall prey to your thoughts--let them support you, and you can do anything.

Blame vs. Responsibility Posted on February 19, 2019, 0 Comments

You can round up all the usual suspects.
Point your finger at each one.

Sugar
Fat
Genetics
Dumb Luck
Time or Money
Big Corporations
The Government
Your Job or your Boss
Your Parents or your Partner
Your Doctor, your Coach, your Trainer

The MRI Cannot Tell You Posted on June 18, 2018, 0 Comments

what you had for dinner last week
or that you had a fight with your spouse
or that you go to bed too late
or that you don't like your job
or that you don't drink enough water
or that a parent said "X" runs in the family
or that you exercise too much/not enough/inappropriately.
or that you're worried about finances
or that you have a dysfunctional breathing pattern.

Myofascial Stretch of Bicep Femoris Posted on April 26, 2018, 0 Comments

Instructions:

• Seated with left leg straight in front of you and the right leg bent with the heel at mid-calf.
• Push the left heel away from the body as you drive the left knee toward the floor to get the leg as straight as possible. Invert the left foot (turn the bottom of the foot toward the right) strongly while pulling the toes back toward the knee.
• At the same time, lean forward with the upper body but keep the chest elevated (don't round the back--keep chest elevated). The right arm should be extended straight in front of the body with the hand in external rotation (palm up and fingertips facing down--like spiderman shooting a webs out of the wrist).
• Once the stretch is felt, turn your body toward the extended leg (left in this example), accentuating the stretch. Your right arm will likely be pointing across the left leg a bit.
• Hold for 30s and then repeat on the other side for 30s, doing 3 repeats each  side.

Artificial Sweeteners, Gut Health, and Obesity Posted on April 22, 2018, 0 Comments

The artificial sweetener acesulfame potassium affects the gut microbiome and body weight gain in CD-1 mice

• Xiaoming Bian,
• Liang Chi,
• Bei Gao,
• Pengcheng Tu,
• Hongyu Ru,
• Kun Lu

Abstract

Artificial sweeteners have been widely used in the modern diet, and their observed effects on human health have been inconsistent, with both beneficial and adverse outcomes reported. Obesity and type 2 diabetes have dramatically increased in the U.S. and other countries over the last two decades. Numerous studies have indicated an important role of the gut microbiome in body weight control and glucose metabolism and regulation. Interestingly, the artificial sweetener saccharin could alter gut microbiota and induce glucose intolerance, raising questions about the contribution of artificial sweeteners to the global epidemic of obesity and diabetes. Acesulfame-potassium (Ace-K), a FDA-approved artificial sweetener, is commonly used, but its toxicity data reported to date are considered inadequate. In particular, the functional impact of Ace-K on the gut microbiome is largely unknown. In this study, we explored the effects of Ace-K on the gut microbiome and the changes in fecal metabolic profiles using 16S rRNA sequencing and gas chromatography-mass spectrometry (GC-MS) metabolomics. We found that Ace-K consumption perturbed the gut microbiome of CD-1 mice after a 4-week treatment. The observed body weight gain, shifts in the gut bacterial community composition, enrichment of functional bacterial genes related to energy metabolism, and fecal metabolomic changes were highly gender-specific, with differential effects observed for males and females. In particular, ace-K increased body weight gain of male but not female mice. Collectively, our results may provide a novel understanding of the interaction between artificial sweeteners and the gut microbiome, as well as the potential role of this interaction in the development of obesity and the associated chronic inflammation.

 

Original Source found here: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0178426

An Examination by Physicians of Flu Vaccine Effectiveness Posted on November 05, 2017, 0 Comments

Thermography and Mammography Posted on October 19, 2017, 0 Comments

THE USE OF THERMOGRAPHY IN DETECTION OF METASTATIC BREAST CANCER

CORINNE FARRELL, M.D., JOHN D. WALLACE, A.B. and CARL M. MANSFIELD, M.D.

ABSTRACT :

Our experience to date has shown that total body thermography can be an aid in the search for metastatic disease in patients with carcinoma of the breast. In our series of 126 patients, we found a true positive rate of 87 per cent, a false negative rate of 3 per cent, and the false positive rate was approximately 10 per cent. Of considerable interest were 7 false positive thermograms which were converted to true positives in 3 to 6 months after the original study.

We have found total body thermography useful in locating the site and extent of a primary lesion, a second carcinoma of the breast or recurrent anti metastatic lesions. It has also been an aid in differentiating associated benign disease. This examination is inexpensive, consumes little time, causes no patient discomfort and has the added advantage of no exposure to ionizing radiation. This technique is capable of detecting early manifestations of metastatic disease, but such manifestations of disease should be confirmed by conventional techniques at this time.

BREAST THERMOGRAPHY AFTER FOUR YEARS AND 10,000 STUDIES

HAROLD J. ISARD, M.D., WARREN BECKER, M.D., RUTH SHILO, M.D. and BERNARD J. OSTRUMM.D.

ABSTRACT :

A total of approximately 10,000 breast thermograms was analyzed and further subdivided into symptomatic and asymptomatic groups of patients of 55 and 45 per cent, respectively.

Positive, or abnormal, mammatherms were recorded in 36 per cent of thesymptomatic and 23 per cent of the asymptomatic groups. Of the 306 histologically confirmed cancers, 270 were in the symptomatic group of patients and 36 were clinically occult.

Clinical accuracy was enhanced by the supplemental use of mammography and thermography. Sixty-one per cent of the occult cancers were suspect by thermography and if, in the asymptomatic group, thermography had been used as the initial screening procedure and mammography performed only on those with abnormal thermograms a yield of 21.4 cancers per 1,000 mammographic examinations would have been realized.

Thermography is an innocuous examination that can be utilized for preliminary screening of asymptomatic women to focus attention upon those who should be examined more intensively because of greater risk of breast cancer.

Efficacy of Computerized Infrared Imaging Analysis to Evaluate Mammographically Suspicious Lesions

1. R. Parisky¹, A. Sardi², R. Hamm³, K. Hughes⁴, L. Esserman⁵, S. Rust⁶ and K. Callahan⁷

ABSTRACT :

OBJECTIVE. The purpose of this clinical trial was to determine the efficacy of a dynamic computerized infrared imaging system for distinguishing between benign and malignant lesions in patients undergoing biopsy on the basis of mammographic findings.

SUBJECTS AND METHODS. A 4-year clinical trial was conducted at five institutions using infrared imaging of patients for whom breast biopsy had been recommended. The data from a blinded subject set were obtained in 769 subjects with 875 biopsied lesions resulting in 187 malignant and 688 benign findings. The infrared technique records a series of sequential images that provides an assessment of the infrared information in a mammographically identified area. The suspicious area is localized on the infrared image by the radiologist using mammograms, and an index of suspicion is determined, yielding a negative or positive result.

RESULTS. In the 875 biopsied lesions, the index of suspicion resulted in a 97% sensitivity, a 14% specificity, a 95% negative predictive value, and a 24% positive predictive value. Lesions that were assessed as false-negative by infrared analysis were microcalcifications, so an additional analysis was performed in a subset excluding lesions described only as microcalcification. In this restricted subset of 448 subjects with 479 lesions and 110 malignancies, the index of suspicion resulted in a 99% sensitivity, an 18% specificity, a 99% negative predictive value, and a 27% positive predictive value. Analysis of infrared imaging performance in all 875 biopsied lesions revealed that specificity was statistically improved in dense breast tissue compared with fatty breast tissue.

CONCLUSION. Infrared imaging offers a safe noninvasive procedure that would be valuable as an adjunct to mammography in determining whether a lesion is benign or malignant.

Microwave thermography in the detection of breast cancer

AH Barrett, PC Myers and NL Sadowsky

ABSTRACT :

Microwave thermography, a method of sensing subcutaneous temperatures, was used in a breast cancer detection study of about 5,000 female patients. The data were taken at wavelengths of 9.1 and 23 cm. Microwave thermography at 23 cm has true-positive and true-negative detection rates of 0.8 and 0.6, respectively, comparable to those of infrared thermography (0.7) and inferior to those of xeromammography (0.9). However, a potential advantage results if microwave and infrared thermography are used together for screening, and if mammography is used only for follow-up on those patients who were positive on either the microwave or the infrared thermograms. It is then possible to obtain true-positive and true-negative detection rates of 0.9 and 0.9, respectively, while only half the number of patients need be subjected to x-rays.

Effectiveness of a noninvasive digital infrared thermal imaging system in the detection of breast cancer.

Arora N, Martins D, Ruggerio D, Tousimis E, Swistel AJ, Osborne MP, Simmons RM.

BACKGROUND: Digital infrared thermal imaging (DITI) has resurfaced in this era of modernized computer technology. Its role in the detection of breast cancer is evaluated.

METHODS: In this prospective clinical trial, 92 patients for whom a breast biopsy was recommended based on prior mammogram or ultrasound underwent DITI. Three scores were generated: an overall risk score in the screening mode, a clinical score based on patient information and a third assessment by artificial neural network. 

RESULTS: Sixty of 94 biopsies were malignant and 34 were benign. DITI identified 58 of 60 malignancies, with 97% sensitivity, 44% specificity, and 82% negative predictive value depending on the mode used. Compared to an overall risk score of 0, a score of 3 or greater was significantly more likely to be associated with malignancy (30% vs 90%, P < .03).

CONCLUSION: DITI is a valuable adjunct to mammography and ultrasound, especially in women with dense breast parenchyma.

 

http://www.nejm.org/doi/full/10.1056/NEJMoa1206809#t=article

Effect of Three Decades of Screening Mammography on Breast-Cancer Incidence

Archie Bleyer, M.D., and H. Gilbert Welch, M.D., M.P.H.

N Engl J Med 2012; 367:1998-2005November 22, 2012

Our study raises serious questions about the value of screening mammography. It clarifies that the benefit of mortality reduction is probably smaller, and the harm of overdiagnosis probably larger, than has been previously recognized. And although no one can say with certainty which women have cancers that are overdiagnosed, there is certainty about what happens to them: they undergo surgery, radiation therapy, hormonal therapy for 5 years or more, chemotherapy, or (usually) a combination of these treatments for abnormalities that otherwise would not have caused illness. Proponents of screening should provide women with data from a randomized screening trial that reflects improvements in current therapy and includes strategies to mitigate overdiagnosis in the intervention group. Women should recognize that our study does not answer the question “Should I be screened for breast cancer?” However, they can rest assured that the question has more than one right answer.

 

http://www.cochrane.org/CD001877/BREASTCA_screening-for-breast-cancer-with-mammography

Screening for breast cancer with mammography

Screening with mammography uses X-ray imaging to find breast cancer before a lump can be felt. The goal is to treat cancer earlier, when a cure is more likely. The review includes seven trials that involved 600,000 women in the age range 39 to 74 years who were randomly assigned to receive screening mammograms or not. The studies which provided the most reliable information showed that screening did not reduce breast cancer mortality. Studies that were potentially more biased (less carefully done) found that screening reduced breast cancer mortality. However, screening will result in some women getting a cancer diagnosis even though their cancer would not have led to death or sickness. Currently, it is not possible to tell which women these are, and they are therefore likely to have breasts or lumps removed and to receive radiotherapy unnecessarily. If we assume that screening reduces breast cancer mortality by 15% after 13 years of follow-up and that overdiagnosis and overtreatment is at 30%, it means that for every 2000 women invited for screening throughout 10 years, one will avoid dying of breast cancer and 10 healthy women, who would not have been diagnosed if there had not been screening, will be treated unnecessarily. Furthermore, more than 200 women will experience important psychological distress including anxiety and uncertainty for years because of false positive findings.

Women invited to screening should be fully informed of both the benefits and harms. To help ensure that the requirements for informed choice for women contemplating whether or not to attend a screening programme can be met, we have written an evidence-based leaflet for lay people that is available in several languages on www.cochrane.dk. Because of substantial advances in treatment and greater breast cancer awareness since the trials were carried out, it is likely that the absolute effect of screening today is smaller than in the trials. Recent observational studies show more overdiagnosis than in the trials and very little or no reduction in the incidence of advanced cancers with screening.

Insights into Bike Myths and Truths (part 3) Posted on June 10, 2017, 0 Comments

As far as strength, the strength required to pedal a bicycle at 300 watts and 90rpms is about the same force that is required to stand up from a chair. It's close to a 45lb single leg press. Something the vast majority of humans can easily accomplish one time without taxing the ability to produce force very much at all. In other words, we are not talking about all that much force, and hardly anyone is anywhere near force or strength limited when riding a bike. What does limit us is the ability to produce that force 90x a minute for multiple minutes or hours. Otherwise known as aerobic capacity.

RESPONSE (a long one BTW) It's like you've read my first book! But just in case, here's a quote:

"Strength, as defined by Bompa in Periodization: Theory and Methodology of Training, is “the neuromuscular capability to overcome an external and internal resistance.” The strength of an athlete is determined by how much work that athlete can perform. In triathlon, then, the competitor must be strong enough to complete the distance. So if you cross the finish line, is this strong enough?

No matter where you placed in your last tri, you covered the same distance as all the other competitors. You got the work done. As a matter of fact, since you all completed the same course, it could be said that you are all equally strong. But that would be inaccurate.

Let’s say that you’re a Clydesdale who always wins his category but just misses out on taking the overall title. So you cherrypick a small Olympic distance race in the middle of nowhere and peak for it like it’s the World Championships. You’ve visualized this race a thousand times and already have a spot picked out for the overall trophy on your wall of fame. You’re gonna rock!

And then I show up.

I live nowhere near the race venue. But I happen to be attending my grandmother’s ninetieth birthday party and hear about this race at the last minute while stopping to use the bathroom at the local Waffle Hut which is sponsoring the event (I wouldn’t eat there!). You see me in the transition area and immediately mark me as possible competition. After all, I have a carbon-fiber Cervelo and the absence of a mullet makes me conspicuous among the rest of the field. But at a buck thirty, I’m not an impressive figure, so you’re not terribly worried as we wade out into the water together.

And then I beat you.

Only by a second or two, but I beat you. You put a minute on me out of the water. Then I catch you on the bike, hammering back to transition to start the run with almost a two-minute advantage. Your long legs eat up most of my lead during the final leg, but, in the end, you run out of real estate and cross the finish a few steps behind me. You’re bummed but console yourself with the knowledge that you made me work for the win, saying you simply lost to a stronger athlete.

How wrong you are.

You weigh two hundred pounds. I weigh 130. We both covered the same distance. But you had to carry an additional seventy pounds over the course of the race. Technically, you did more work. Work is force applied over distance. It is the product of the amount of resistance overcome (two hundred pounds vs. 130 pounds) and the distance over which that resistance is moved (an Olympic distance triathlon). You are the stronger athlete. Strap a seventy-pound weight to my body, and I would probably still be at the bottom of the lake somewhere.

I know, I’m not making much of a case for strength training here. I mean, if it’s not the strongest athlete who wins, why lift weights, right? If you’re thinking like that, I can tell you’ve skipped the first several chapters of this book. There’s a multitude of reasons, but let’s look at strength and its critical role in the performance of a triathlon.

If we change some of the parameters of the imaginary race cited above, it may provide you with a clearer understanding of the importance of strength in our sport. Let’s say I let myself go a bit during the off season—to the tune of seventy pounds. I win a year’s supply of Breyer’s Mint Chocolate Chip and decide I’m going to test out the Ullrich Theory of Performance Enhancement. We both show up on the starting line, but this time I’m two hundred pounds, same as you. You win the race walking away, with a personal best of two hours even. I score a different type of PR—four hours. You probably could’ve lapped me if you’d run the course a second time. Obviously you’re the stronger athlete now, right?

Wrong again.

Once more, we both completed the same distance. Yet now we weigh the same. We both did the same work. It doesn’t matter if I took twice as long as you to cover the distance, as time is a variable which does not enter into the strength equation. Time is important in the equation for power. By the strictest definition of strength, we are both equal despite the fact you had enough time to shower, eat, and overhaul your bottom bracket before I crossed the finish line.

Why then, are we wasting our time on strength development? Why not just skip to power training (no pun intended) if that’s what’s really going to determine who finishes a particular race in first place?

Power is how much work is done per unit of time or, expressed as an equation:

POWER = [FORCE (i.e., strength) x DISTANCE]/TIME

The reason triathletes must first focus on strength is because this biomotor ability is a crucial component in the optimal development of power. Tudor Bompa, in his groundbreaking book Periodization: Theory and Methodology of Training, agrees. Strength development, he says, “should be the prime concern of anyone who attempts to improve an athlete’s performance.” Its importance is again highlighted on a page from Advanced Program Design, which states, “When strength or any of its derivatives are the primary deficit, efforts should focus primarily on its development first.” Thus, to maximize power development, we must either maximize strength or maximize speed, or, with a good training program, maximize both.

Maximum Strength is the highest force that can be performed by the neuromuscular system during a maximum voluntary contraction.

FORCE = MASS x ACCELERATION (F = M x A)

So to increase the force produced, we can increase the resistance (M) or the speed at which the resistance is moved (A). Yet increasing movement speed is not as effective in the development of maximum strength as increasing the weight of the resistance, due primarily to the role momentum plays in the lift.

Momentum is mass in motion. For those of you who fell asleep in physics class, I’ll keep this simple. The more mass or velocity an object has, the more momentum that object will possess. That’s one reason why you see some people swinging their free weights around and rushing through a set of twelve like their lives depend on it. The only newton they’ve ever heard of is a cookie. But they innately know that once they start their hundred-pound bicep curl with their back and knees, their arms can be along for the ride. Momentum is their ego’s best friend.

Maximal tension on a muscle, which is critical for maximal strength development, is only increased during the initial acceleration of the load. After that, momentum takes over and effectively reduces the tensile loading of the muscle. But if you use a sufficiently heavy weight, the speed at which the weight is lifted will be limited. Thus, the contribution of momentum to the lift will be minimized, as well.

This is not to say that you should not try to accelerate the load as quickly as possible. To quote Chek again, “The closer a given load is moved to maximum velocity the greater the intensity and the greater the training effect on a neuromuscular basis.” The neuromuscular benefits to which Chek refers are:

increased neural drive to the muscle
increased synchronization of motor units
increased activation of the contractile apparatus
decreased inhibition of the protective mechanisms of the muscle (Golgi tendon organ).

Basically, you’re making the muscle smarter when you challenge it with a sufficient resistance, literally putting brains behind that brawn. And a smart, functional muscle is a strong muscle.

Strength is, ironically, often an endurance athlete’s biggest weakness. But the intelligent triathlete quickly learns to apply this one golden rule: Train your weaknesses and race your strengths."

Again, I am not really trying to argue with Andrew, because I can't. He knows more about the body than me by orders of magnitude. In the end, we are all after the same thing, results. And that is my battleground. Exercise physiologists, physical therapists and the larger research community have always lagged behind real coaches. Great coaches find performance, and then everyone else figures out how they did it. While not able to hold my own in any body knowledge debate, what I would certainly do is rest my case for simplicity on the performance of my athletes, the results of my bike fits, and my excellent record of not injuring the vast majority of them along the way.

RESPONSE: While admitting I lag behind many people in various areas, I need to clarify I actually have SOME knowledge of coaching/training. In fact, I can honestly say that of the many people who grace my client roster, some are quite accomplished in their various sporting endeavors. For the sake of brevity, I'll focus on the endurance athletes I've worked with--including professional cyclists, national champions both in the US and abroad, winners of both stages and the overall of some UCI level races. Heck, I even recall working with a Grand Tour Winner. I daresay some of them might even go so far as to call me a decent coach/trainer. Does that make me anybody to listen to--nope! What does, perhaps, is having studied and practiced under some of the greatest minds in the fields of human performance and health and then practicing what I preach so I end up being more than just a talking head, academic with no real, practical experience. Even then, I encourage whoever may be listening to not believe anything I've said until they've learned it properly and applied it to themselves. Take the knowledge off the page and do something with it before claiming to know it. And even then, realize there's always more to learn. One of the reasons I've actually enjoyed this exchange with you, Dave. Now, I do qualify for a free bike fit and it would be fun to continue this discussion in person. But I've been fitted by Matt Cole himself. And my riding time is, sadly, limited these days. Guess I'm spending too much time on FB. I'll give you the last word, though (as you can see) I've used most of them. If you've read this far, I applaud you. Your endurance is likely surpassed by few.

Insights into Bike Myths and Truths (part 2) Posted on June 10, 2017, 0 Comments

This is a continuation of an earlier blog post, the first part of which can be found here:

https://triumphtraining.com/blogs/blog/insights-into-bike-myths-and-truths-part-1

These are some really good examples of how individuals thoroughly (and properly) trained in how the body works, can take that information and thoroughly complicate the simple act of pedaling a bike.

RESPONSE: As a cyclist pedals, the majority of force production is provided by the quadriceps, which extend the knee approximately 74° from 111° flexion to 37°. During extension, the knee also adducts due to the normal valgus angulation of the distal femoral condyles in relation to the foot/pedal interface during the downstroke. This causes medial translation of the knee as it extends. In addition, pronation of the foot coupled with internal tibial rotation increases stress on the medial knee. We have not even considered the roles of the vestibular components or how the various organ systems of the body are impacted as well as impact the act of pedaling a bike. Simple--I think that's not the most accurate descriptor.

"Just starting at #1, that's a great theory and probably true, except it never happens. Pedaling a bike with a crank arm 2.5-10mm shorter is so entirely similar to pedaling at the longer crank length that phrases such as " will likely cause a decrease in performance (e.g. power) in the short term until the body has acquired the ability to perform the new skill(s) autonomously." simply does not apply after the first 30 seconds. Body knowledge says it should, while thousands of real world examples say otherwise. Crank length change is below the threshold of mattering for anything beyond the positive change to thigh-torso clearance."

RESPONSE: An organism, when stressed, often reverts what it knows. It's why habits (even bad ones) can be hard to break. Survival is the driver here. The subconscious believes the reason you've alive despite all the challenges to that survival are because of the actions you've taken in the past--even if those actions haven't served you. Thus, it's very difficult to learn a new skill when the organism is under stress. It's also extremely difficult to practice a newly acquired skill when the system is continually stressed. Exercise is a stress. So even if you have a certain form that is more efficient/powerful, as you become increasingly fatigued the ability to use the new form/position/equipment decreases as the body goes back to what has gotten it this far in the first place. Thus, I don't doubt that after 30s a cyclist you've fitted on shorter crank arms sees some benefit. But at 30s, that's roughly 45 revolutions per leg. What type of impact do you think that has on the neural pathways of a cyclist who's pedaled 10hrs/week in a certain position with certain equipment for a decade? That's 520hrs in a year which equates to 31,200 minutes. In 10 yrs, that's 312,000 minutes. At approximately 90 "reps" per leg, that cyclist has a different motor ingram that has been ingrained in his neuromuscular system some 28,080,000 times. EACH LEG! My bet, is the cyclist might have some "issues" maintaining the same level of performance he achieved during the 30s of your test.

The funny thing is, I was actually agreeing with you on this point, simply saying there will be an initial and temporary drop off in performance even if the change is, ultimately, going to result in an improvement. Of course, there comes a point when an improvement will not occur if the cyclist has found the length which works best for his/her physiology/chosen race. So I encourage a more cautious approach when using absolutes like "never" and the like. It demonstrates a keen inability to engage in anything other than linear thinking when a complexity model would likely serve you better.

For 2,3 & 4, I can't argue with Andrew, but I don't need to. There are multiple studies on changing cadence and modifying your force application beyond simple alternating pushes. The vast majority show a decrease in efficiency. How to pedal a bike in a steady state, time trial effort is pretty settled science. Track riders, sprinters, super high power instances and low traction situations are exceptions, that rarely apply to my target audience. The exception is not the rule.

RESPONSE: I was pretty sure your target audience was mostly multisport athletes. But because the initial observations were so general, I had to point out that--like anything--it depends. And again, I would be careful with info obtained simply from studies. Learning to interpret studies and their inherent limitations if not outright falsifications at times is an excellent skill to have. Just don't try to acquire it if your system is currently being stressed. However, if you'd like, here's some research you may find enlightening:

"As these cyclists have to engage in single-legged cycling, they have to generate force on the pedal with just one limb throughout the whole pedal cycle. This is going to result in a lower peak power (Bundle et al., 2006), as well as an increased time to peak power through a combination of the use of one limb (Bundle et al., 2006) and being seated as opposed to standing (Bertucci et al., 2005; Padulo et al., 2014). The exercising muscle mass is required to generate more force throughout the pedal cycle in one-legged compared to two-legged cycling resulting in a higher mechanical and metabolic load (Abbiss et al., 2011). However, the differential VO2uptake to one- vs. two-legged exercise suggests that there may be a circulatory inhibitory response to two vs. one-legged exercise (Ogita et al., 2000), and one-legged sprint cycling relying less on anaerobic metabolism than two-legged cycling (Bundle et al., 2006), this may contribute to different fatigue profiles in the C2 class. Additionally, single-legged cycle training can result in significant improvements in the oxidative and metabolic potential of skeletal muscle in trained cyclists (Abbiss et al., 2011)."

5. I addressed this, but to restate, I never suggested that riding a trainer or always using a super controlled environment was the way. What I said was ALL of those other skills and adaptations are relatively quickly and easily addressed, when compared to the scope and magnitude of aerobic development that can be better achieved in those super controlled environments.

RESPONSE: God, we agree on too much. The trainer is an excellent and, in general, the most efficient way to develop the aerobic system (with the added bonus of catching up on video coverage of races you may have missed). Indeed, when used correctly, I estimate that 1hr inside = 1.5hrs outside. So it's great for the working, time-crunched athlete. And for triathletes, whose race demands are not the same as road/mtb/track cyclists it may even be ideal. However, I would argue that anyone who claims skills such as riding in a tightly bunched group (which you've never experienced unless you've raced professionally abroad or in any of the World Tour races which take place on US soil) and descending at speed or cornering in adverse conditions can be easily addressed has never, in fact, actually done so. If you'd like to follow me down a rainy mountain pass in Spain sometime, I'd be happy to have you on my wheel.

6. Specific adaptations to imposed demands indeed. The primary demands of climbing a hill are light weight and high power. The secondary ones are gearing, pacing, "mental fortitude", and actually climbing a few hills to know how it feels and engage slightly different muscles slightly differently a small portion of the time. The only argument I make is (again) let's stop turning secondary demands into primary ones. The exception is not the rule.

RESPONSE: I think we're moving in circles here (but...that's better than squares to continue the cycling analogy). I assume most people coming to be fit by you have a bike. A secondary demand would be a good fit. I bet the reason these folks choose you is the secondary demand is appealing enough so they'll pay to have the benefit of your expertise. Put two cyclists with the exact same attributes/experience on bikes--one fit by you and one fit by Walmart--my money is on your guy. My money is also on the guy who has spent some time addressing these "secondary" demands I mention above.

7&8 Yay! We agree!

RESPONSE: Excellent as I'm starting to develop calluses from typing.

9. I think we agree here as well, but just to be sure.... Adaptation to climatic conditions is fast. Aerobic development is slow. The exception is not the rule.

RESPONSE: See my comment in #6 above.

10. "Flexibility/stability need to be developed before strength which needs to be developed before power." Again, I can't argue with this, but I don't have to. Flexibility is rarely a limiter in developing a world class bike position. It just isn't. In other words, it is not that hard to ride a bike in the same position as the best in the world. Most of us have the chassis to do so, but we lack the engine to go as fast. A tri bike is the most athletically demanding of all bikes, and even there, most riders can get national caliber results with the biggest limited not being flexibility / mobility / stability / strength / power, but far more often the 20 extra lbs hanging around their mid section.

RESPONSE: With all due respect, most folks chassis are out of alignment; quite often, severely so. In fact, I've never assessed a client--from stay-at-home moms to professional football players--that didn't have multiple dysfunctions which needed to be addressed. In regards to your target audience, I'll quote my book: "Flexibility is the ability to adapt to changes in position or alignment, allowing us to perform joint actions through a wide range of motion. Often used interchangeably with mobility, which can be defined as the ability to move freely, these two concepts are the heart of this chapter. They’re also the heart of the biomotor abilities above. Think about it—how agile can you be if your muscles are stiff? Have you ever cramped during a triathlon? Your ability to move or change direction quickly was instantly curtailed. In fact, if you weren’t stopped dead in your tracks, you probably looked like the Tin Man trying to jog a couple of days after hanging out in the rain all night. Being too tight also affects your balance. Pulled out of ideal alignment by tonic musculature, you are literally over-committed in one direction. Coordination will suffer, too, as a lack of mobility must be compensated for elsewhere in the kinetic chain, often resulting in inefficiency and injury. With altered length/tension relationships, the triathlete must now work harder to perform a given movement which adversely affects endurance. Muscles positioned outside of their optimal strength curve will not only be weaker but, since strength is a component of power, a final injustice to the inflexible triathlete is that these last two biomotor abilities will never reach their full potential—much like this triathlete and his placement in the overall field."

The phase "going lower isn't always faster" is without a doubt true. Here is a phrase that is 'more' true. "Going lower is usually faster." The exception is not the rule, and we need to consider the target audience.

Age group triathletes hear that 1st statement and sabotage themselves as they come into a bike fit determined to not ride "too low". Of course, simply bending them over to the will of the bike fitter is not the process. Taking them down, forward and adjusting crank length to achieve the lowest position where pedaling mechanics, breathing and digestion can be maintained is the goal. Anything higher than that is less aero the vast majority of the time. That is what the wind tunnel says, and barring a trip to t he wind tunnel, our best approach during a bike fit is to play the odds.

RESPONSE: Agree again--play the odds. But if we're just using odds without thinking, then I can have a monkey fit me with the same chances of any improvement. And, again, the funny thing is, I was actually agreeing with your original point.

The blog post is continued (yes, again) in Part 3.

Insights into Bike Myths and Truths (part 1) Posted on June 10, 2017, 0 Comments

A cycling friend of mine, who happens to be one of the best fitters in the U.S., asked me my opinion on the following observations made on FaceBook:

For the record, I WHOLLY OR MOSTLY DISAGREE with each of the following statements, and more importantly, could point you to peer reviewed scientific studies to back up my positions on most of them.
1. Shortening your crank arm will cause you to lose power.
2. "Scraping mud", "powering the upstroke", "making perfect circles", or any other technique advice beyond "push hard" is the correct method to pedal.
3. There is a performance benefit to changing your cadence from what feels natural (usually raising the cadence).
4. One legged pedaling is a good drill.
5. Riding a trainer doesn't prepare you to ride outside.
6. You need to climb hills to get better at climbing hills.
7. Road bikes climb better.
8. Road bikes are faster for some triathlon courses.
9. Train outside year round to stay heat acclimated.
10. Increasing your flexibility will allow a better aerobar position, usually referring to hamstring flexibility as it relates to aerobar drop.

My response:

1--The Law of Facilitation states that once an impulse travels through a given set of neurons, it will tend to do so at a future date. And each time it traverses the path, the resistance will be less. Basically, practice makes perfect. Or more accurately, practice makes permanent. Thus, any change, even for the better, will likely cause a decrease in performance (e.g. power) in the short term until the body has acquired the ability to perform the new skill(s) autonomously.

2--Depends on what the goal is. If you simply want to produce the most power, "push hard" is probably a decent idea. However, if your goal is efficiency over a given distance, an ability to respond to attacks/changes of pace, maintain traction/control over unstable surfaces, or running off the bike to your potential, the ability to apply force (notice, I'm not saying MAX force) anywhere/anytime during the pedals stroke and have a variety of different muscles contribute synergistically is a good skill. Like learning how to drive, taking martial arts, etc., learning begins at slower speeds (e.g. cadence) until proficiency allows for replication of the acquired skill at higher speeds/subconscious levels. This is one of the reasons why better sustained power numbers are easier to see when climbing at lower cadences--the cyclist doesn't have the neuromuscular efficiency (i.e., skill) to pedal with the same quality at higher cadences. And while I could give anyone examples for each of the above goals, remember it is the ENTIRE body that pedals the bike--not simply the legs. You may find this blog post of interest here: https://triumphtraining.com/.../8139819-cycling-evolution

3--It depends on what the goal is again. And the point made in #1 above is applicable here, too. Hell, terrain needs to be considered; temperature and humidity play a role. Additionally, the biomechanics, muscle fiber type, training history--even the hormonal profile of the cyclist in question are factors to consider when choosing the optimal cadence. That being said, power is (roughly) an equation of cadence x gear size. Increase one or increase the other or increase both. The limiting factor in gear size is typically the muscular system while the limiter in cadence is often the aerobic system. Neither system works independently from the other, of course. And neuromuscular efficiency is a component of both systems. While both the muscular/aerobic systems have genetic caps (which most of us will never come close to finding), the neuromuscular system can always become more efficient.

4--if you need it, yes. See #2 above. Also #3's reference to efficiency of the neuromuscular system. Again, note that it is the whole body (including all of its systems) which propels the bike and these limiters are often revealed as well as trained during the course of one-legged pedaling drills.

5--aerobically, it does. But it doesn't prepare you (optimally) for descending at speed, cornering in wet conditions, bumping shoulders at 40mph with 200 other cyclists, bunny hopping pot holes, curbs, or even fallen riders, or any of the other "skills" a cyclist is forced to address if you ride/compete enough. I can tell you that racing in America is different than racing in Europe. And while, like the trainer, it's better than nothing, ultimate adaptation doesn't happen until you're exposed to the specific stimulus. Train exclusively on the trainer and then go do an average Belgian kermesse. You'll get yourself dropped out of fear if you don't crash yourself (and others) first.

6--you don't NEED to. Is it the most efficient way? Perhaps. Are there changes in many if not most aspects of riding on the flats vs. riding on a climb--yes, including mental ones. Specific adaptation to Imposed Demands. Wanna get good at climbing? Climb. Wanna get even better at climbing? Stop eating crap and ignoring the Foundational Factors of Health while working on power:weight ratio, and you'll see improvements regardless of terrain or chosen sport.

7--depends again. Not when the fit is right or the person is adapted to a particular position.

8--if the course is straight up and the person is accustomed to riding the road bike, yes. Otherwise, a properly fit tri bike will be faster.

9--if your race is in the cold, acclimate for the cold. If it's in the heat, acclimate to the heat. Heat can be MUCH more of an issue when riding inside if you want it to be--and a huge advantage both physically and (more importantly) mentally for those who are adapted to hot/humid conditions. Note, however, quality sessions performed exclusively in "hard" conditions will likely result in an athlete sacrificing quality and, therefore, not realizing their full potential. Consider the adage of sleep high/train low. Same goes for temperatures.

10--Flexibility/stability need to be developed before strength which needs to be developed before power. I wrote a whole book on this subject, but I would agree that lower (often predicated on flexibility and core strength) does not mean better in regards to aero position. If you're sacrificing either power or comfort in order to get lower, it's not going to pay the dividend you're looking for as far as results. And aero is more than just low frontal surface area. That being said, if you're limited in flexibility or stability, you will not realize your full potential on the bike or any other discipline. And it's quite likely you'll eventually get injured trying. But if it brings you into my studio, that injury could be the best thing that ever happened to your performance.

The original poster (who is, himself, quite an accomplished bike fitter) then responded with:

These are some really good examples of how individuals thoroughly (and properly) trained in how the body works, can take that information and thoroughly complicate the simple act of pedaling a bike.

Just starting at #1, that's a great theory and probably true, except it never happens. Pedaling a bike with a crank arm 2.5-10mm shorter is so entirely similar to pedaling at the longer crank length that phrases such as " will likely cause a decrease in performance (e.g. power) in the short term until the body has acquired the ability to perform the new skill(s) autonomously." simply does not apply after the first 30 seconds. Body knowledge says it should, while thousands of real world examples say otherwise. Crank length change is below the threshold of mattering for anything beyond the positive change to thigh-torso clearance.

For 2,3 & 4, I can't argue with Andrew, but I don't need to. There are multiple studies on changing cadence and modifying your force application beyond simple alternating pushes. The vast majority show a decrease in efficiency. How to pedal a bike in a steady state, time trial effort is pretty settled science. Track riders, sprinters, super high power instances and low traction situations are exceptions, that rarely apply to my target audience. The exception is not the rule.

5. I addressed this, but to restate, I never suggested that riding a trainer or always using a super controlled environment was the way. What I said was ALL of those other skills and adaptations are relatively quickly and easily addressed, when compared to the scope and magnitude of aerobic development that can be better achieved in those super controlled environments.

6. Specific adaptations to imposed demands indeed. The primary demands of climbing a hill are light weight and high power. The secondary ones are gearing, pacing, "mental fortitude", and actually climbing a few hills to know how it feels and engage slightly different muscles slightly differently a small portion of the time. The only argument I make is (again) let's stop turning secondary demands into primary ones. The exception is not the rule.

7&8 Yay! We agree!

9. I think we agree here as well, but just to be sure.... Adaptation to climatic conditions is fast. Aerobic development is slow. The exception is not the rule.

10. "Flexibility/stability need to be developed before strength which needs to be developed before power." Again, I can't argue with this, but I don't have to. Flexibility is rarely a limiter in developing a world class bike position. It just isn't. In other words, it is not that hard to ride a bike in the same position as the best in the world. Most of us have the chassis to do so, but we lack the engine to go as fast. A tri bike is the most athletically demanding of all bikes, and even there, most riders can get national caliber results with the biggest limited not being flexibility / mobility / stability / strength / power, but far more often the 20 extra lbs hanging around their mid section.

The phase "going lower isn't always faster" is without a doubt true. Here is a phrase that is 'more' true. "Going lower is usually faster." The exception is not the rule, and we need to consider the target audience.

Age group triathletes hear that 1st statement and sabotage themselves as they come into a bike fit determined to not ride "too low". Of course, simply bending them over to the will of the bike fitter is not the process. Taking them down, forward and adjusting crank length to achieve the lowest position where pedaling mechanics, breathing and digestion can be maintained is the goal. Anything higher than that is less aero the vast majority of the time. That is what the wind tunnel says, and barring a trip to t he wind tunnel, our best approach during a bike fit is to play the odds.

We want to also drop the upper back and head down between the shoulder blades, but that is a secondary concern to getting the rider as low as we can while maintaining the abilities of pedaling, breathing, digesting.

As far as strength, the strength required to pedal a bicycle at 300 watts and 90rpms is about the same force that is required to stand up from a chair. It's close to a 45lb single leg press. Something the vast majority of humans can easily accomplish one time without taxing the ability to produce force very much at all. In other words, we are not talking about all that much force, and hardly anyone is anywhere near force or strength limited when riding a bike. What does limit us is the ability to produce that force 90x a minute for multiple minutes or hours. Otherwise known as aerobic capacity.

Again, I am not really trying to argue with Andrew, because I can't. He knows more about the body than me by orders of magnitude. In the end, we are all after the same thing, results. And that is my battleground. Exercise physiologists, physical therapists and the larger research community have always lagged behind real coaches. Great coaches find performance, and then everyone else figures out how they did it. While not able to hold my own in any body knowledge debate, what I would certainly do is rest my case for simplicity on the performance of my athletes, the results of my bike fits, and my excellent record of not injuring the vast majority of them along the way.

To which I then replied with an extensive thread that you'll find in Part 2 of this Blog Post.

The Overlooked Role of Nutrition in Training Induced Fatigue Posted on April 09, 2017, 0 Comments

Missed my morning FaceBook post due to a 90+ mile bike ride, but it served as motivation for what to write about today.

One of the amino acids which even the most nutritionally ignorant among us has heard of is tryptophan. After all, that's what makes you sleepy after that turkey dinner on Thanksgiving, right? Well, not exactly. But that's not my point.

Tryptophan is the precursor for the neurotransmitter 5-hydroxytryptamine (5-HT), which is involved in fatigue. It's also one of the primary amino acids released when muscle is catabolized during times when fuel is inadequate to meet the demands placed on an organism's physiology. In the case of my group ride this morning, there were many examples of people getting tired. Some of those cyclists could blame their training, of course. Others, however, need to consider how their fueling strategy--both on AND off the bike--might be contributing to their fatigue at a given intensity/duration. When glucose levels/glycogen stores are not sufficient to keep muscle (along with free fatty acids, primarily in the form of PUFAs) from being catabolized to fuel the activity, performance of the activity will suffer or stop altogether.

And if you think about it, it's simply another ingenious example of the body trying to survive. The body believes that fuel is scarce. It has no idea you could simply stop at the next convenience store and buy a coke or, better yet, some o.j. But since you won't stop, you body stops you. Or slows you down--anything it can do to spare the body's limited resources. And it has a lot of built in safeguards at play in these conditions just in case. From the production of serotonin (not the happy hormone you've been led to believe) to the inhibition of glucose utilization via the Randle Cycle, the body's gonna win this one. So you can live to ride another day.

And this time, maybe you'll fuel yourself appropriately.

Glucose Deprivation--it's not sweet if you're concerned about Alzheimer's Posted on February 02, 2017, 0 Comments

Abstract

Glucose deficit triggers tau pathology and synaptic dysfunction in a tauopathy mouse model

Clinical investigations have highlighted a biological link between reduced brain glucose metabolism and Alzheimer’s disease (AD). Previous studies showed that glucose deprivation may influence amyloid beta formation in vivo but no data are available on the effect that this condition might have on tau protein metabolism. In the current paper, we investigated the effect of glucose deficit on tau phosphorylation, memory and learning, and synaptic function in a transgenic mouse model of tauopathy, the h-tau mice. Compared with controls, h-tau mice with brain glucose deficit showed significant memory impairments, reduction of synaptic long-term potentiation, increased tau phosphorylation, which was mediated by the activation of P38 MAPK Kinase pathway. We believe our studies demonstrate for the first time that reduced glucose availability in the central nervous system directly triggers behavioral deficits by promoting the development of tau neuropathology and synaptic dysfunction. Since restoring brain glucose levels and metabolism could afford the opportunity to positively influence the entire AD phenotype, this approach should be considered as a novel and viable therapy for preventing and/or halting the disease progression.

“Glucose deficit triggers tau pathology and synaptic dysfunction in a tauopathy mouse model” by E Lauretti, J-G Li, A Di Meco & D Praticò in Translational Psychiatry. Published online January 31 2017 doi:10.1038/tp.2016.296

Original source found here: http://www.nature.com/tp/journal/v7/n1/full/tp2016296a.html

Another Study about the Dark Side of Serotonin Posted on August 29, 2016, 0 Comments

Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala

 

Serotonin (also known as 5-hydroxytryptamine (5-HT)) is a neurotransmitter that has an essential role in the regulation of emotion. However, the precise circuits have not yet been defined through which aversive states are orchestrated by 5-HT. Here we show that 5-HT from the dorsal raphe nucleus (5-HTDRN) enhances fear and anxiety and activates a subpopulation of corticotropin-releasing factor (CRF) neurons in the bed nucleus of the stria terminalis (CRFBNST) in mice. Specifically, 5-HTDRN projections to the BNST, via actions at 5-HT2C receptors (5-HT2CRs), engage a CRFBNST inhibitory microcircuit that silences anxiolytic BNST outputs to the ventral tegmental area and lateral hypothalamus. Furthermore, we demonstrate that this CRFBNST inhibitory circuit underlies aversive behaviour following acute exposure to selective serotonin reuptake inhibitors (SSRIs). This early aversive effect is mediated via the corticotrophin-releasing factor type 1 receptor (CRF1R, also known as CRHR1), given that CRF1R antagonism is sufficient to prevent acute SSRI-induced enhancements in aversive learning. These results reveal an essential 5-HTDRN→CRFBNST circuit governing fear and anxiety, and provide a potential mechanistic explanation for the clinical observation of early adverse events to SSRI treatment in some patients with anxiety disorders.

 

Original Source found HERE: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature19318.html

Everything You Know About Nutrition is Wrong Posted on July 20, 2016, 1 Comment

Everything you know about nutrition is wrong.

But maybe you knew that already.  Maybe you find yourself smack dab in the category of “Normal American” and realize the company you keep isn’t the healthiest in the world.  More than two thirds of your peers are overweight.  And looking in the mirror you realize these folks are your peers for a reason.  You should have been devastated to learn you’d been diagnosed with cancer; but then again, so have more than half the people you know.  Terms like hypertension and diabetes roll off your tongue like you just graduated from med school.  You and your friends discuss irritable bowel with a whiff of…umm…well…authority.  And the truth is you’re popping so many pills for a litany of symptoms your doctor often asks you if a certain prescription may be right for him.   You have a sneaking suspicion that it’s all caused by diet.  And I’m here to tell you it’s time to go with your gut.

Or at least stop working against it, for goodness sake! 

Eight of the top ten leading causes of death* in the United States can be attributed to what we’re eating in this country.  

1. Heart Disease
2. Cancer
3. Chronic lower respiratory disease
4. Accidents (unintentional injuries)
5. Stroke
6. Alzheimer’s disease
7. Diabetes
8. Influenza and pneumonia
9. Kidney disease
10. Suicide

 

*Annually there are around 2,596,993 deaths registered in the US with the leading top 10 causes accounting for nearly 75% of all deaths.

 

Sometimes that connection is rather obvious (if not misconstrued), as is the case with heart disease and diabetes.  Other times the association is a bit more ambiguous.  How cancer or Alzheimer’s disease is impacted by diet and gut health has only recently been explored by modern medicine.  Yet over a hundred years ago, the relationship between a healthy digestive system and the overall health of the human organism had already been well established:

 

“In mammals there exist two brains of almost equal importance to the individual and race.  One is the cranial brain, the instrument of volitions, of mental progress and physical protection.  The other is the abdominal brain, the instrument of vascular and visceral function.  It is the automatic, vegetative, the subconscious brain of physical existence.  In the cranial brain resides the consciousness of right and wrong.  Here is the seat of all progress, mental and moral ... However, in the abdomen there exists a brain of wonderful power maintaining eternal, restless vigilance over its viscera.  It presides over organic life.  It dominates the rhythmical function of viscera....The abdominal brain is a receiver, a reorganizer, an emitter of nerve forces.  It has the power of a brain.  It is a reflex center in health and disease....The abdominal brain is not a mere agent of the [cerebral] brain and cord; it receives and generates nerve forces itself; it presides over nutrition.  It is the center of life itself.  In it are repeated all the physiologic and pathologic manifestations of visceral function (rhythm, absorption, secretion, and nutrition).  The abdominal brain can live without the cranial brain, which is demonstrated by living children being born without cerebrospinal axis.  On the contrary the cranial brain can not live without the abdominal brain....”  (Robinson, 1907, pp. 123 -126)

 

Byron Robinson’s book, The Abdominal and Pelvic Brain, wasn’t well ahead of its time.  We’ve simply become so focused in this age of specialization that we’ve lost sight of anything “proven” outside the confines of the laboratory environment.  Still, science trudges inexorably forward, eventually returning to what primitive societies have innately known for eons:

what we eat matters

Weston A. Price was another health pioneer who gained invaluable insights into the truth of that statement by daring to study the real world.  His research in the 1920s and 1930s took him all over the globe, eventually culminating in his seminal work, Nutrition and Physical Degeneration.   Dr. Price spent years not just studying but living with, talking to, and even assimilating the cultures and habits of numerous indigenous peoples.  He wanted to understand why Modern Man was so afflicted with numerous diseases while traditional societies remain largely unaffected.  His book chronicled, both in word and pictures, the decline in health as people adopted a diet of convenient, processed foods. 

Today it’s even worse.  Over 70% of the food consumed in the Western diet didn’t exist 10,000 years ago which probably means you weren’t designed to eat it.  And much like putting diesel in an engine built for unleaded fuel, consuming foods not optimal for our metabolic machinery degrades our function on every level.  A dentist, Price concentrated much of his research on oral health; and many contemporary studies share a similar focus:

 

These results support notions that a decrease in masticatory stress among agriculturalists causes the mandible to grow and develop differently. This developmental argument also explains why there is often a mismatch between the size of the lower face and the dentition, which, in turn, leads to increased prevalence of dental crowding and malocclusions in modern postindustrial populations.

 

Other researchers looked beyond the mechanical repercussions on the oral cavity, considering symptoms which were literally less “in your face”:

 

IBS is one of the most common functional gastrointestinal disorders worldwide and is thought to be the result of disturbed neural function along the brain-gut axis….studies have demonstrated that IBS may be associated with an activated adaptive immune response. Increased epithelial barrier permeability and an abnormal gut flora might lead to increased activation of the intestinal immune system.

 

The Enteric Nervous System (ENS) is a subdivision of the Autonomic Nervous System (ANS).  Formed early in embryonic development, the ENS is located in the sheaths of gastrointestinal tissue lining the esophagus all the way down to the anus.  It is estimated to have between 200 and 600 million neurons—more than the entire spinal cord—proof if its importance in the evolution of the human organism.  Though able to function entirely independently of the Central Nervous System (CNS), the ENS connects to the CNS via the vagus nerve, constantly supplying the brain with information coming from the various components of the gastrointestinal tract. 

One of the critical pieces of data being relayed along this pathway is the health of bacteria residing in the intestines.  You are a body of over 100 trillion cells.  Yet you have more bacteria in your gut than you have cells in your body.  An estimated four pounds of bacteria are found in the intestines of the average adult, 85% of which should be “good” while the remaining 15% are considered “bad” or harmful.  Unfortunately, as this microorganism population becomes imbalanced, so does the biochemistry of the brain. 

Recent studies have implicated the health of the intestinal flora in various mood disorders and abnormal mental states, including clinical depression.  The authors of a 2011 review of the scientific literature regarding the ENS write, “this link may contribute to several neuropsychiatric disorders, emphasizing the key role of nutrition….”

And though Dr. Price may not have practiced during an era in which the term “gut-brain axis” was a part of the medical vernacular, he most definitely recognized how poor diet encouraged physical, mental, and moral deterioration.  Chapter 19 of Nutrition and Physical Degeneration opens with:

 

After one has lived among the primitive racial stocks in different parts of the world and studied them in their isolation, few impressions can be more vivid than that of the absence of prisons and asylums.

 

Is it plausible that our gut influences our thoughts and our emotions?  Is it possible that how we eat could truly affect how we act and behave—so much so that our diet determines our destiny?  Our morals molded by macronutrients?

Well, the reverse is certainly true.  Our mental state continually impacts the function of our digestive system. Do you ever get “butterflies” before an important presentation or performance?  Have you ever gotten so nervous before a competition you felt sick to your stomach.  Where do you think the term “scared shitless” comes from?  All are examples of the enteric nervous system responding to signals from the brain, the study of which is exploding in the new field of neurogastroenterology.  The gut gets feedback from the brain. And science is beginning to conclude that this communication is bi-directional—the brain’s biochemistry reflects the biochemistry of the gut—a novel hypothesis gaining ground as research and common sense inevitably converge:

 

Genetic and environmental studies implicate immune pathologies in schizophrenia. The body's largest immune organ is the gastrointestinal (GI) tract. Historical associations of GI conditions with mental illnesses predate the introduction of antipsychotics. Current studies of antipsychotic-naïve patients support that gut dysfunction may be inherent to the schizophrenia disease process. Risk factors for schizophrenia (inflammation, food intolerances, Toxoplasma gondii exposure, cellular barrier defects) are part of biological pathways that intersect those operant in the gut. Central to GI function is a homeostatic microbial community, and early reports show that it is disrupted in schizophrenia. Bioactive and toxic products derived from digestion and microbial dysbiosis activate adaptive and innate immunity.

 

The critical gut-brain axis is finally garnering the scientific attention it deserves as serious flaws in the conventional, allopathic model of medicine are being discovered.  People are sick and tired of being sick and tired with the “this” for “that” approach too often leaving patients with more of “that”. 

We are our own worst enemies when we allow recommendations made by experts with specific agendas, financial, political, or otherwise to guide us.  And until we realize that blindly following double blind studies instead of our intuition—that instinct which has been developed and refined during hundreds of thousands of years of not just survival but evolution as well—until we honor the guru in our gut, we will never truly be healthy. 

Ultimately, we can be our own best therapists. 

Even though the state of our intestinal flora is predicated on far more than what we eat, returning to a more traditional diet is still a powerful strategy to reclaim the health that is our birthright.  Basically, just eat whatever your grandparents would recognize as food.  And if you don’t know what that might have been, simply do the opposite of every recommendation ever made by any government agency or corporate product in the past 70 to 100 years.  If you want more specifics, you could get a copy of my book—Spot On: Nutrition.  Or read some of the articles coming out in future blog posts and past ones, too.  Either way, you’re taking responsibility for yourself, and I bet your head will resonate with that decision. 

I know your gut will.   

Fiber Fibs Posted on April 12, 2016, 0 Comments

Stopping or reducing dietary fiber intake reduces constipation and its associated symptoms

AIM: To investigate the effect of reducing dietary fiber on patients with idiopathic constipation.

METHODS: Sixty-three cases of idiopathic constipation presenting between May 2008 and May 2010 were enrolled into the study after colonoscopy excluded an organic cause of the constipation. Patients with previous colon surgery or a medical cause of their constipation were excluded. All patients were given an explanation on the role of fiber in the gastrointestinal tract. They were then asked to go on a no fiber diet for 2 wk. Thereafter, they were asked to reduce the amount of dietary fiber intake to a level that they found acceptable. Dietary fiber intake, symptoms of constipation, difficulty in evacuation of stools, anal bleeding, abdominal bloating or abdominal pain were recorded at 1 and 6 mo.

RESULTS: The median age of the patients (16 male, 47 female) was 47 years (range, 20-80 years). At 6 mo, 41 patients remained on a no fiber diet, 16 on a reduced fiber diet, and 6 resumed their high fiber diet for religious or personal reasons. Patients who stopped or reduced dietary fiber had significant improvement in their symptoms while those who continued on a high fiber diet had no change. Of those who stopped fiber completely, the bowel frequency increased from one motion in 3.75 d (± 1.59 d) to one motion in 1.0 d (± 0.0 d) (P < 0.001); those with reduced fiber intake had increased bowel frequency from a mean of one motion per 4.19 d (± 2.09 d) to one motion per 1.9 d (± 1.21 d) on a reduced fiber diet (P < 0.001); those who remained on a high fiber diet continued to have a mean of one motion per 6.83 d (± 1.03 d) before and after consultation. For no fiber, reduced fiber and high fiber groups, respectively, symptoms of bloating were present in 0%, 31.3% and 100% (P < 0.001) and straining to pass stools occurred in 0%, 43.8% and 100% (P < 0.001).

CONCLUSION: Idiopathic constipation and its associated symptoms can be effectively reduced by stopping or even lowering the intake of dietary fiber.

INTRODUCTION: Lack of fiber in the diet was first postulated in 1971 as the cause of diseases such as diverticulosis, hemorrhoids and colorectal cancer[1]. Since then, partly due to widespread media publicity, it is now widely accepted that dietary fiber is a necessary component of a healthy diet and is required for normal bowel movement[2-5]. It is popularly used in the management of constipation by the public and by many doctors. Insoluble fiber is known to increase stool weight and decrease colonic transit time[6,7]. Fiber is said to aid in water retention in the colon and results in stools that are less dry and easier to evacuate. However, the reality is that stool moisture content remains at 70%-75% regardless of the amount of fiber and water consumed[7,8].

There is recent evidence that low fiber intake does not equate to constipation[9]. Patients with chronic constipation also have similar fiber intake to controls[10-13]. Patients with chronic constipation may also have worsening symptoms when dietary fiber intake is increased[14]. Another study found that lactulose was more effective in easing constipation when compared with fiber[15].

It has also been our experience that many patients with constipation are already consuming a large amount of fiber before they seek medical attention.

We therefore carried out a prospective longitudinal case study to investigate the effect of decreasing dietary fiber in patients with idiopathic constipation.

MATERIALS AND METHODS: Constipation was defined clinically in patients who presented either with symptoms of straining to expel bulky large stools or a bowel frequency of less than one motion per 3 d over a period of at least 3 mo. Patients who presented to the clinic with symptoms of constipation, abdominal distension, pain or bloating, difficulty in evacuation with or without symptoms of rectal bleeding were considered for the study. For the purpose of this study, we did not distinguish between slow colonic transit type or obstructed defecation type of constipation nor did we attempt to classify the patients according to irritable bowel syndrome subtypes. All the patients underwent colonoscopy to exclude colonic lesions. Patients who had colorectal cancer, previous colonic surgery, melanosis coli or thyroid disorders were excluded. Patients with anal conditions such as severe prolapsed hemorrhoids, chronic anal fissure or any other condition that required surgery were also excluded.

Sixty-three consecutive patients after normal colonoscopy were enrolled into the study from May 2008 to May 2010. Each patient was to act as their own control. The physiology of the gastrointestinal tract and the bulking effects of dietary fiber were explained to the patients[16,17]. Patients were then instructed to completely stop their intake of dietary fiber, including vegetables, cereals, fruits, wholemeal bread and brown rice for 2 wk. Those who were vegetarians were asked to eat white rice instead of unpolished rice, white bread instead of whole meal bread, and to take processed bean products for protein. They were to continue their normal quantities of carbohydrates and proteins. Sieved fruit juices and clear vegetable soups were allowed. Patients were instructed not to take any laxatives during these 2 wk. After 2 wk, patients were asked to continue on with as little fiber in their diet as they were comfortable with for the long term. Patients were followed up at 1 mo and 6 mo intervals and final results were analyzed at 6 mo.

Data collected included age, sex, general dietary fiber intake, symptoms of constipation, difficulty in evacuation of stools, anal bleeding, abdominal bloating or abdominal pain. Constipation was recorded as the interval in days between bowel movements. Difficulty in evacuation was a subjective measure and patients were asked to choose from one of 3 degrees (no straining, occasional or moderate straining and severe straining or straining most of the time).

RESULTS: There were 16 males (25.6%) and 47 (74.4%) females, median age 47 years (range, 20-80 years) included in the study. At the commencement of the study, all patients were already on a high fiber diet or taking fiber supplements. After 2 wk of a no fiber diet, patients were asked to continue on as little fiber in the diet as they were able to follow if this were to give them relief from their symptoms.

At 6 mo, 41 patients continued on a no fiber diet and 16 were on a reduced fiber diet. The remaining 6 patients continued on a high fiber diet for various reasons including being vegetarians or inability to stop consuming dietary fiber for religious or personal reasons.

The median age of patients who stayed on a no fiber diet was 46 years (range, 21-80 years), on a reduced fiber diet was 45 years (range, 20-65 years) and on a high fiber diet was 59 years (range, 28-75 years). There was no statistical significant difference in age between the 3 groups. There was also no statistical difference in sex between the 3 groups.

At 6 mo follow-up, the interval between bowel movements decreased with the reduction in fiber intake (P < 0.001). Forty one patients who completely stopped fiber intake had their bowel frequency increased from one motion in 3.75 d (± 1.59 d) to one motion in 1.0 d (± 0.00 d) (P < 0.001). Of 16 patients who reduced their dietary fiber intake, 12 patients had daily bowel movement, 3 had one bowel movement every 2 to 3 d and one had a bowel movement every 4 to 6 d, giving one motion per 1.9 d (± 1.21 d) on a reduced fiber diet compared with 1 motion per 4.19 d (± 2.09 d) on a high fiber diet (P < 0.001). There was no change in the frequency of bowel movement for patients who continued with high dietary fiber intake, with one motion per 6.83 d (± 1.03 d) before and after consultation (P = 1.00).

There was also a difference between the groups in the proportion of patients with associated symptoms. For symptoms of bloating, all of those on a high fiber diet continued to be symptomatic, while only 31.3% in the reduced fiber group and none of the no fiber group had symptoms.

With regards to straining, all those on a no fiber no longer had to strain to pass stools. Of those who reduced dietary fiber, 7 of 16 showed improvement while the symptoms remain unchanged in those who remained on a high fiber diet (P < 0.001 between groups).

Symptoms of abdominal pain only improved in patients who stopped fiber completely while those who continued on a high fiber diet or reduced fiber diet did not show any improvement (Table ​(Table2).2). In addition, those on a no dietary fiber diet no longer had symptoms of anal bleeding.

DISCUSSION: This study has confirmed that the previous strongly-held belief that the application of dietary fiber to help constipation is but a myth. Our study shows a very strong correlation between improving constipation and its associated symptoms after stopping dietary fiber intake. However whilst there was no significant difference between the mean age of the 3 groups with different post-consultation dietary fiber intake, older patients seemed less likely to stop dietary fiber, although this did not reach significance. We did not survey the actual reasons for resuming dietary fiber. The clinical impression during consultation however was that some of these patients were vegetarians, some felt uneasy not eating any fiber, whilst others could not completely discontinue fiber due to constant media and peer pressure to increase dietary fiber.

Constipation is often mistaken by the layman as the state of not passing stool, with the subsequent false notion that making more feces will allow easier defecation. In truth, constipation refers to the difficulty in evacuating a rectum packed with feces, and easier defecation cannot possibly be affected by increasing dietary fiber which increases bulky feces. In this paper, we looked at constipation both as the number of days before each motion as well as the ease of defecation.

It is well known that increasing dietary fiber increases fecal bulk and volume. Therefore in patients where there is already difficulty in expelling large fecal boluses through the anal sphincter, it is illogical to actually expect that bigger or more feces will ameliorate this problem. More and bulkier fecal matter can only aggravate the difficulty by making the stools even bigger and bulkier. Several reviews and a meta-analysis had already shown that dietary fiber does not improve constipation in patients with irritable bowel diseases[18-21].

The role of dietary fiber in constipation is analogous to cars in traffic congestion. The only way to alleviate slow traffic would be to decrease the number of cars and to evacuate the remaining cars quickly. Should we add more cars, the congestion would only be worsened. Similarly, in patients with idiopathic constipation and a colon packed with feces, reduction in dietary fiber would reduce fecal bulk and volume and make evacuation of the smaller and thinner feces easier. Adding dietary fiber would only add to the bulk and volume and thus make evacuation even more difficult.

Whilst it is often stated in physiology textbooks that bulking agents improve peristalsis, there is no proof of this in practice nor experimentally. Regardless of the food ingested, small intestinal and right mid colonic contents are fluid and all ingestible dietary fiber is suspended therein. Dietary fiber, therefore, cannot act as solid boluses for the initiation of peristalsis. In fact, dietary fiber had been shown to retard peristalsis and hold up gaseous expulsion in human experiments[22].

Dietary fiber is also associated with increased bloatedness and abdominal discomfort[22]. Insoluble fiber was reported to worsen the clinical outcome of abdominal pain and constipation[18-20]. In our recent study, patients who followed a diet with no or less dietary fiber intake showed a significant improvement, not just in their constipation, but also in their bloatedness. Patients who completely stopped consuming dietary fiber no longer suffered from abdominal bloatedness and pain. These symptoms are caused by the fermentation of dietary fiber by colonic bacteria, which produces hydrogen, carbon dioxide and methane[23]. Gases that are trapped by peristaltic colon exert pressure on the walls, causing the abdominal pain experienced by patients. This was previously observed in a prior study on younger patients, when dietary fiber had been shown not to be effective in the management of children with recurrent abdominal pain or bloating[21].

Stools only become well-formed in the sigmoid colon and rectum and by this time, especially in constipated subjects, more stools result in more evacuation problems. It is not logical to increase both the volume and size of stool in patients with idiopathic constipation and indeed for anybody with difficulty in passing stools, e.g., due to anismus or anal spasm from anal stricture, fissure or pelvic outlet disorders. We have shown that decreasing the bulk and volume of feces immediately enables the easier evacuation of smaller and thinner stools through the anal sphincter mechanism. This eliminates the need to strain in passing stools, and prevents the tearing of the anal sphincter and bleeding due to large and bulky fecal loads. None of our patients experienced anal bleeding or straining following complete abstinence from dietary fiber.

The results of this study should lead us to reexamine popular beliefs in benefits of dietary fiber and more studies should be undertaken to confirm or repudiate these results.

In conclusion, contrary to popularly held beliefs, reducing or stopping dietary fiber intake improves constipation and its associated symptoms.

Original Source found here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435786/

Cholesterol and Parkinson's Disease Posted on April 07, 2016, 0 Comments

Mov Disord. 2015 Apr;30(4):552-9. doi: 10.1002/mds.26152. Epub 2015 Jan 14.
Statins, plasma cholesterol, and risk of Parkinson's disease: a prospective study.

Abstract

Previous findings on the association of statins, plasma lipids, and Parkinson's disease (PD) are confounded by the fact that statins also affect lipid profiles. We prospectively examined plasma lipids and statin use in relation to PD in the Atherosclerosis Risk in Communities (ARIC) Study. Statin use and plasma lipids were assessed at baseline (visit 1, 1987-89) and at three triennial visits thereafter (visits 2-4) until 1998. Potential PD cases were identified from multiple sources and validated where possible. The primary analysis was limited to incident PD cases diagnosed between 1998 and 2008. Odds ratios and 95% confidence intervals were derived from multivariate logistic regression models. Statin use was rare at baseline (0.57%) but increased to 11.2% at visit 4. During this time frame, total-cholesterol levels decreased, particularly among statin users. Fifty-six PD cases were identified after 1998. Statin use before 1998 was associated with significantly higher PD risk after 1998 (odds ratio = 2.39, 95% confidence interval 1.11-5.13) after adjusting for total cholesterol and other confounders. Conversely, higher total cholesterol was associated with lower risk for PD after adjustment for statin usage and confounders. Compared with the lowest tertile of average total cholesterol, the odds ratios for PD were 0.56 (0.30-1.04) for the second and 0.43 (0.22-0.87) for the third tertile (P(trend) = 0.02). Statin use may be associated with a higher PD risk, whereas higher total cholesterol may be associated with lower risk. These data are inconsistent with the hypothesis that statins are protective against PD.

 

Original Source found here: http://www.ncbi.nlm.nih.gov/pubmed/25639598

Vegetarian Diet and Gene Mutation Posted on March 30, 2016, 0 Comments

Original Source: http://www.nzherald.co.nz/lifestyle/news/article.cfm?c_id=6&objectid=11613993

Vegetarianism can lead to heart disease and cancer

By Sarah Knapton 2:38 PM Wednesday Mar 30, 2016

 

Long term vegetarianism can lead to genetic mutations that raise the risk of heart disease and cancer, scientists have found.

Populations who have had a primarily vegetarian diet for generations were found to be far more likely to carry DNA that makes them susceptible to inflammation.

Scientists in the US believe that the mutation occurred to make it easier for vegetarians to absorb essential fatty acids from plants.

But it has the knock-on effect of boosting the production of arachidonic acid, which is known to increase inflammatory disease and cancer. When coupled with a diet high in vegetable oils - such as sunflower oil - the mutated gene quickly turns fatty acids into dangerous arachidonic acid.

The finding may help explain previous research which found vegetarian populations are nearly 40 per cent more likely to suffer colorectal cancer than meat eaters, a finding that has puzzled doctors because eating red meat is known to raise the risk.

Researchers from CornellUniversity in the US compared hundreds of genomes from a primarily vegetarian population in Pune, India to traditional meat-eating people in Kansas and found there was a significant genetic difference.

"Those whose ancestry derives from vegetarians are more likely to carry genetics that more rapidly metabolise plant fatty acids," said Tom Brenna, Professor of Human Nutrition at Cornell.

"In such individuals, vegetable oils will be converted to the more pro-inflammatory arachidonic acid, increasing the risk for chronic inflammation that is implicated in the development of heart disease, and exacerbates cancer. The mutation appeared in the human genome long ago, and has been passed down through the human family."

To make the problem worse, the mutation also hinders the production of beneficial Omega 3 fatty acid which is protective against heart disease. Although it may not have mattered when the mutation first developed, since the industrial revolution there has been a major shift in diets away from Omega 3 - found in fish and nuts - to less healthy Omega 6 fats - found in vegetable oils.

"Changes in the dietary Omega 6 to Omega 3 balance may contribute to the increase in chronic disease seen in some developing countries," added Dr Brenna. "The message for vegetarians is simple. Use vegetable oils that are low in omega-6 linoleic acid such as olive oil." (I would add that avoidance of PUFAs in general is a good strategy, replacing them in the diet with saturated fat from quality sources). 

The mutation is called rs66698963 and is found in the FADS2 gene which controls the production of fatty acids in the body.

Previous studies have shown that vegetarianism and veganism can lead to problems with fertility by lowering sperm counts. (Nature doesn’t want to perpetuate weakness.  Thus, anytime one’s vitality sinks below the level where one can positively contribute to the gene pool, the ability to procreate is compromised or lost entirely). 

Separate research from Harvard University also found that a diet high in fruit and vegetables may impact fertility because men are consuming high quantities of pesticides.

Many vegetarians also struggle to get enough protein, iron, vitamin D, vitamin B12 and calcium which are essential for health. One study found that vegetarians had approximately five percent lower bone-mineral density (BMD) than non-vegetarians.

However other research suggests vegetarianism lowers the risk of diabetes, stroke and obesity.

The new research was published in the journal Molecular Biology and Evolution

 

Original Study can be accessed here: http://mbe.oxfordjournals.org/content/early/2016/03/09/molbev.msw049.full.pdf+html

Positive selection on a regulatory insertion-deletion polymorphism in FADS2 influences apparent endogenous synthesis of arachidonic acid

 

Abstract

Long chain polyunsaturated fatty acids (LCPUFA) are bioactive components of membrane phospholipids and serve as substrates for signaling molecules. LCPUFA can be obtained directly from animal foods or synthesized endogenously from 18 carbon precursors via the FADS2 coded enzyme. Vegans rely almost exclusively on endogenous synthesis to generate LCPUFA and we hypothesized that an adaptive genetic polymorphism would confer advantage. The rs66698963 polymorphism, a 22 bp insertion-deletion within FADS2, is associated with basal FADS1 expression, and coordinated induction of FADS1 and FADS2 in vitro. Here we determined rs66698963 genotype frequencies from 234 individuals of a primarily vegetarian Indian population and 311 individuals from the U.S. A much higher I/I genotype frequency was found in Indians (68%) than in the U.S. (18%). Analysis using 1000 Genomes Project data confirmed our observation, revealing a global I/I genotype of 70% in South Asians, 53% in Africans, 29% in East Asians, and 17% in Europeans. Tests based on population divergence, site frequency spectrum and long-range haplotype consistently point to positive selection encompassing rs66698963 in South Asian, African and some East Asian populations. Basal plasma phospholipid arachidonic acid status was 8% greater in I/I compared to D/D individuals. The biochemical pathway product-precursor difference, arachidonic acid minus linoleic acid, was 31% and 13% greater for I/I and I/D compared to D/D, respectively. Our study is consistent with previous in vitro data suggesting that the insertion allele enhances n-6 LCPUFA synthesis and may confer an adaptive advantage in South Asians because of the traditional plant-based diet practice.