WALLETECTOMY

 

When I was a kid food was different.  We didn’t have much packaged food.  We were 6 in my family so meals had to be affordable.  My Mom mostly made soups and stews or meat and vegetables.  We were rarely allowed sugary foods – only on birthdays. That included soda.  My Mom had a craving for salt so she would order Charles Chips by the container and sometimes their pretzels. (But those were mostly for her and she kept them hidden for special treats.)  Fruit was our snack.  Nobody in our family was overweight.  Thank you Mom!

Recently (the last decade) I’ve had the amazing opportunity to study lifestyle genetics.  I find I have all the carb sensitivity gene mutations (proven with clinical studies) and many of the fat sensitivity gene mutations.  I have blood sugar mutations.  I have a profile that would set me up to be overweight if all of those genes expressed but because my Mom had us on a low glycemic eating program, they did not express.

When I went to college I went “hog wild” and ate packaged crumb cakes, cookies, all kinds of carbs and drank soda.  No surprise I gained 25 pounds.  I managed to lose it all by taking up racquetball and for 30 years I maintained my weight with exercise.

Last year my Mom died. She had just turned 88 and had blocked arteries. Her first symptom was extreme pain. She was told she had shingles. I suggested she have a stress test.  They found the blockages.

She was recommended open heart surgery.  I work with many kinds of health professionals.  Not one of them thought that was a good idea.  If she did not have the surgery she would die.  But we (the health professionals and myself) all felt if she did have the surgery, she would not recover and the end would be beyond miserable.  My siblings encouraged her to have the surgery, I believe out of their own desire to keep her alive but also because the hospital MDs said she could make it.  They likely knew she could not survive this surgery.  They also most likely knew what her end would be like.

So why would they do that?

That is what my best friend calls a “walletectomy.”  I don’t blame MDs.  They have to follow hospital protocols or they can get sued.

So why is it the hospital protocol?

That brings us to the United States medical system.  You can’t avoid politics if you are talking about health.  The U.S is the only western country that doesn’t take care of its citizens’ health.  Right now they want to downgrade the little care they do offer.  Why?  Because the current administration values the support of business more than they value the quality of life of their citizens regardless of the spin they constantly put out.  And BTW, the alternative to truth is falsehood.

But, I digress….

After my Mom’s surgery she told me she was being “blamed” for not trying to do the exercises and recovery routines they recommended.  During this time her organs were all struggling to recover.

I’m pretty sure my Mom continued her low glycemic style of eating most of her life but I learned eventually she was an alcoholic – the secret kind.  It’s always a clue when someone BRINGS alcohol with them to visit you.  Just in case…

The point of my story is I BELIEVE in low glycemic lifestyle. Alcohol is not part of it. Alcohol will make you fat and it will contribute to heart disease.  It also puts you at a higher risk for cancer.

Once in a while is a good rule for most things.  I have a glass of red wine maybe 3 times per year and I can only drink about an inch of it because I have liver detox mutations and a whole glass will give me a hangover. Yuk.  What is once in a while for you?

I’d suggest once/week.

If you can’t do that, I’d suggest you ask yourself why.

I’m a super enthusiastic proponent of the TLS system for weight management and healthy cardiovascular system.  I highly recommend you watch this video and then do the quiz.  Does it cost money?  Yes.  Is it worth it?  YES YES YES!!!!  I will personally help you to be accountable on a daily basis, no fee.  This will be the last program you will every need to get fit. I’ll add one caveat – IF YOU ARE READY to stop yo yo-ing.

It would be my pleasure to speak to you.

If you are a health professional who would like to be the health leader you know you can be, implement epigenetics, weight management, prevention, etc. ….

It would be my pleasure to offer a complementary proposal and the support you deserve.

Kathy@criticalhealth.org, 617.515.7559.

Below is more information on cardiovascular support and weight management for the science minded, clinically trained.  This infographic is also for women. Women can commit domestic violence, assault, be aggressive, etc.

An article by Dr. David Brownstein, (MD),03/18/17 about using cholesterol to diagnose heart disease

In an on-line article in The New York Times today (3.17.17), the headline states, “Cholesterol-Slashing Drug Can Protect High-Risk Heart Patients, Study Finds.”  The article describes the first test of the new cholesterol-lowering medication—Repatha.  Repatha is part of the PCSK9 inhibiter family that works by lowering LDL-cholesterol levels through poisoning an enzyme—PCSK9–thereby allowing LDL receptors to remain in circulation.  LDL receptors can bind LDL-cholesterol, thus more LDL receptors will result in lowered LDL-cholesterol levels.

 

I have written about PCSK9 inhibitors before.  In my book, The Statin Disaster, I wrote, “I do not think PCSK9 inhibitors will be an effective treatment for heart disease as it will disrupt a normal physiologic process in the body: the binding of LDL to its receptor.” (1) So, let’s look at the first study which was published in the New England Journal of Medicine, March 17, 2017. This was a randomized, double-blind, placebo controlled trial involving 27,564 subjects with heart disease and LDL-cholesterol of 70 mg/dl or higher who were receiving statin therapy.

The primary endpoint was the composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization.  Keep in mind that hospitalization for angina and coronary revascularization (i.e., coronary artery bypass graft surgery or stent placement) are considered soft endpoints since the decision to hospitalize or place a stent is a subjective decision by the physician.  The ultimate success of any cardiac medication should be based on hard endpoints such as death, heart attacks, or stroke.

After 48 weeks of Repatha therapy or placebo, the authors reported that, compared to placebo, the Repatha group significantly reduced the risk of the primary end point by 15% (9.8% in the treatment group vs. 11.3% in the placebo group.)  However, as I have pointed out to you before, the 15% reduction is actually a relative risk reduction.  The relative risk is a statistical term that has no meaning when considering whether to recommend or not recommend a therapy to a patient.  A more accurate assessment is the absolute risk difference.  In this case, the absolute risk difference between the two groups is 1.5%.  A more accurate description of the results should state: as compared to placebo, taking Repatha for two years’ results in a 1.5% decline in a combination of outcomes including death, stroke, myocardial infarction, hospitalization for angina and coronary revascularization.  Another way to look at the data is that the drug failed 98.5% who took it as they received no benefit.  And, if you take out the soft endpoints, the 1.5% decline disappears.

I called Specialty Pharmacy to find out how much Repatha costs.  I was told Repatha costs $2,351.05 per month for a total of $28,212.60/year). So, a two-year course of the medication costs $56,425.20.  (Note; The NYT article states the drug costs $14,523 per year.)

For the physicians, out there, I have a question for you:  Who the heck would prescribe an expensive drug, associated with serious adverse effects, that fails 98.5% who take it?

For the patients, out there I have a question for you:  Who the heck would spend $28,212.60/year for a drug that is associated serious side effects and fails 98.5% who take it?  In this study 25% of those that received Repatha reported serious adverse effects.     What were the serious adverse effects?  I don’t know—they weren’t listed individually.

Repatha is another example about what is wrong with conventional medicine. President Trump just released his first budget.  I would advise him to start tweeting about the failure of Repatha and why it should not be allowed in the market place.  There are far too many ineffective, expensive drugs right now.  We don’t need another one.  Statins are a great example of ineffective drugs that fail nearly 99% who take them.  Now we can add PCSK9 inhibitors to the pile of poorly-performing drugs.

More information about cholesterol lowering medications can be found in my book, The Statin Disaster.

Repatha for heart disease?  Fugetaboutit!

The Triglyceride/HDL Cholesterol Ratio. What Is Ideal?

Many studies have found that the triglyceride/HDL cholesterol ratio (TG/HDL-C ratio) correlates strongly with the incidence and extent of coronary artery disease. This relationship is true both for men and women.

One study found that a TG/HDL-C ratio above 4 was the most powerful independent predictor of developing coronary artery disease.

With the increasing prevalence of overweight, obesity, and the metabolic syndrome this ratio may become even more important because high TG and low HDL-C is often associated with these disorders.

The TG/HDL-C ratio can easily be calculated from the standard lipid profile. Just divide your TG by your HDL-C.

However, when looking at the ideal ratio, you have to check if your lipid values are provided in mg/dl like in the US or mmol/L like in Australia, Canada, and most European countries.

If lipid values are expressed as mg/dl (like in the US);

TG/HDL-C ratio less than 2 is ideal

TG/HDL-C ratio above 4 is too high

TG/HDL-C ratio above 6 is much too high

If you live outside the US or are using mmol/L, you have to multiply this ratio by 0.4366 to attain the correct reference values. You can also multiply your ratio by 2.3 and use the reference values above.

If lipid values are expressed as mmol/L (like in Australia, Canada, and Europe);

TG/HDL-C ratio less than 0.87 is ideal

TG/HDL-C ratio above 1.74 is too high

TG/HDL-C ratio above 2.62 is much too high

My lifestyle genetics

My good friend Nancy Miller-Ilhi, PhD

NIH clinical study LeptiCore


Training, Competition and Genetics

InjuryRiskKK.jpg

The regular demands of training and competition make professional, collegiate, and recreational athletes highly susceptible to injury.

Genetics have a large influence over strength, muscle size and muscle fiber composition (fast or slow twitch), anaerobic threshold (AT), lung capacity, flexibility, power and endurance.

Injury is a fact of life for most athletes, but some professionals—and some weekend warriors —just seem more injury-prone than others. But what is it about their bodies that makes the bones, tendons, and ligaments so much more likely to tear or strain—bad luck, or just poor preparation?

A growing body of research suggests another answer: that genetic makeup may play an important role in injury risk.

Recreational distance running causes high numbers of injuries, with incidence rates estimated between 30% and 75% per person per year.

Treatment of sports injuries costs at least $160 billion per year in the U.S. and Major League Baseball lost $1.6 billion in payroll between 2008 and 2013 because of injuries to players. Avoiding injuries and remaining healthy is key to the success of a team or an individual athlete.

The potential to use genetic testing to reduce sports injuries

 

COL1A1

The COL1A1 gene, for example, encodes the alpha chain of type I collagen, the major protein component of all tendons and ligaments.  It’s associated with vasodilation, blood pressure control, efficiency of muscular contraction and cell hydration.

The GT alleles have a moderately raised risk of tendon and ligament injuries in sport. They need to undertake pre-habilitative exercises relevant to the sports they participate in and consider nutritional support for connective tissue.  They will have reduced response to endurance training and should make sure they stay sufficiently hydrated during endurance activities.

The GG will have an increased risk for tendon and ligament injuries and ruptures and or shoulder dislocations especially related to sports participation. They should also undertake pre-habilitative exercises relevant to the sports they participate in and consider nutritional support for connective tissue. They will have reduced response to endurance training and should make sure they stay sufficiently hydrated during endurance activities.

The TT variants contribute to positive response to endurance training.  They are positive for increased muscle efficiency especially in conjunction with ACE I-allele.  The T allele leads to increased expression of type I collagen alpha polypeptides compared with the G nucleotide, which may increase the tensile strength of tendons and ligaments. About 4% of athletes carry 2 copies of the T allele.

(90% of people who have brittle bone disease have mutations in COL1A1 and COL1A2.  I’m sure these folks would have liked to know early on so they could have taken preventive measures.)

Besides polymorphisms in COL1A1, there are additional DNA variants associated not only with ACL rupture and Achilles tendinopathy but also with other athletic injuries (shoulder dislocations and muscle strain severity).  It is important to note here that there are antibiotics that can flox genes and cause serious injuries, ruptures of the Achilles tendons and other tendons and even disability.  To learn more about fluoroquinolones like Cipro and Levaquin click here.  (Pharmacogenetic screenings can identify contraindication with prescription medications.)

The gene COL5A1 encodes the protein collagen alpha-1(V) chain. It is a minor connective tissue component but of ubiquitous distribution.  Type V collagen binds to DNA, heparin sulfate, thrombospondin, heparin, and insulin.  Defects in COL5A1 are a cause of Ehlers-Danlos syndrome (EDS1).

GDF5

A functional skeletal system requires the coordinated development of many different tissue types, including cartilage, bones, joints, and tendons. Members of the Bone morphogenetic protein (BMP) family of secreted signaling molecules have been implicated as endogenous regulators of skeletal development. This is based on their expression during bone and joint formation, their ability to induce ectopic bone and cartilage, and the skeletal abnormalities present in animals with mutations in BMP family members. One member of this family, Growth/differentiation factor 5 (GDF5).

IL6

 

IL-6 mutations can be involved with other mutations like CRP and TNF in autoimmune disorders like Epstein Barr if the athlete has the mutation and is overtraining.

IL-6R is associated with immune response and cell growth. Dysregulated production of IL6 and this receptor are implicated in the pathogenesis of many diseases, such as multiple myeloma, autoimmune diseases and prostate cancer.

CRP

C-Reactive protein (CRP) is associated with acute phase protein and rises in response to inflammation in the body.  Elevation in CRP concentration will aid in determining the severity of acute tissue injury.

TNF

The genetic variant Tumor Necrosis Factor (TNF) causes over-inflammation. There is data suggesting that TNF may exacerbate neurobehavioral deficits and tissue damage.  If an athlete is over-training it could be involved in autoimmune disease.

Acute traumatic joint injury increases the risk of developing osteoarthritis.  Elevated levels of TNF and IL-6 have been detected in joint injuries.

There are separate studies concerning genetic polymorphisms associated with athletic performance, such as muscle contractility and V̇O2 max. Genetic information of this sort has recently been used to prevent injuries and maximize athletic performance. A professional soccer team in the English Premier League, for example, tested athletes for genetic loci associated with sports performance, and the English Institute of Sport expressed interest in providing genetic testing to Britain’s Olympic athletes in 2012.

The future holds promise for everyone. Someone with limited genetic potential can find ways to compensate and become a solid performer and athletes who are lucky to have exceptional genetics can optimize them.

Trainers and professionals can use this information to help optimize their clients and patients.

I think this is the best genetic lifestyle screening on the market because of the genetic scientist behind it, Dr. Keith Grimaldi.  I know his integrity and ethics.  He will not put genes in his screening that haven’t been tested with 3 independent clinical placebo studies proving a change in genetic expression influenced by a change in lifestyle.

If you would like to integrate this screening into your practice to improve patient outcomes, I’d be happy to offer you a complementary proposal.  Contact me at Kathy@CriticalHealth.org or 617.515.7559.

If you would like to use this screening to develop an action plan for your own optimal health, I’d be happy to offer it to you with my complementary services for a review of results.  Contact me at Kathy@CriticalHealth.org or 617.515.7559.

 

Why Genetic Lifestyle Screening Can Make a Difference

General Timeline of Genetic Training in Sports

1966 – 1991 Y-chromosomal testing as part of official sex segregation.
2001 Policy of the International Association of Athletics Federations and of the International Olympic Committee, respectively.
2001 Professional Boxing and Martial Arts Board of Victoria considers compulsory genetic screening for APOE4 variant in boxers.
2003 World Anti-doping Agency prohibits methods of gene doping.
2005 Eighteen Australian male rugby players were tested and analyzed for 11 genes.

The Chicago Bulls attempt genetic testing of free agent, Eddy Curry, for the purpose of ruling out hypertrophic cardiomyopathy.

2009 23andMe analyzes DNA samples from 100 current and former NFL linemen.

Major League Baseball begins using genetic testing with prospective players from the Dominican Republic and other Latin American Countries.

2010 The National Collegiate Athletic Association implements mandatory sickle cell trait screening.
2011 An English Premier League soccer team analyzes players’ DNA samples at 100 genetic loci.

The National Football League screens for genetic conditions sickle cell trait and G6PD under the 2011 NFL collective bargaining agreement.

2012 2012 English Institute of Sport expresses interest in the integration of genetic technologies to “tailor the training, conditioning, and preparation” of Britain’s Olympic and Paralympic athletes.
2014 Two Barclay’s Premier League soccer teams commission tests of their players’ DNA for 45 variants.


http://bjsm.bmj.com/content/41/8/469.full.pdf
http://journals.lww.com/cjsportsmed/Abstract/2013/01000/Collagen_Genes_and_Exercise_Associated_Muscle.9.aspx

http://www.theatlantic.com/health/archive/2015/02/the-genetics-of-being-injury-prone/385257/

http://www.sciencedirect.com/science/article/pii/S000292970760127X

http://ghr.nlm.nih.gov/gene/COL1A1

https://www.geneticliteracyproject.org/2015/01/08/can-we-yet-use-genetics-to-determine-which-sports-are-best-for-our-kids/

http://sportsmedicine.about.com/od/anatomyandphysiology/a/genetics.htm

http://www.ncbi.nlm.nih.gov/pubmed/22750484

http://www.sciencedirect.com/science/article/pii/S0012160699992412

http://www.ncbi.nlm.nih.gov/pubmed/8959256

http://www.ncbi.nlm.nih.gov/pubmed/23611870

http://www.ors.org/Transactions/55/1056.pdf