Yet, for mammals, lifespan is much shorter. Human beings have a potential lifespan of more than 120 years⁴ which is much shorter than the amazing animals mentioned above but is still remarkable when others, like the common mouse gets only three years⁵. This hardly seems fair to the humble house mouse when its distant relative, the naked mole rat gets closer to 30 years⁶.

Can we change the speed we age?
The deeper you look the clearer it becomes that just like the diversity of life there is a diversity of longevity. And with that realization researchers have rushed to investigate the difference between short and long-lived species to identify and perhaps even develop interventions translating the lessons we learn from research and harnessing them to prolong the years we spend youthful and healthy on this planet.

In 2013 scientists published a paper called the Hallmarks of Aging in a research journal called Cell⁷. This paper identified nine hallmarks or causes of aging that ranged from DNA damage to mitochondrial dysfunction to cellular senescence. Each hallmark qualified as being involved in aging by the results of laboratory experiments. If you made a hallmark worse, it accelerated the aging process and if you protected it, you slowed down the aging process. This paper was important because it gave researchers targets to investigate to see if they could impact aging, and in so doing, they unleashed a phenomenal level of research to find compounds that positively affect each hallmark. And the size of the prize is huge. When a company solves the question of slowing the aging process, it will disrupt a trillion-dollar industry and give birth to a brand new one overnight.

Measuring the speed at which we age
Recently researchers have discovered that we have a biological clock that sits on our DNA with time being recorded by the number of methyl groups attached to our DNA⁸. Using machine learning they identified patterns of methylation that are closely correlated with our chronological age. And in the process discovered that different people age at different speeds not just outwardly but on the inside as well, and measurably so by looking at their DNA methylation patterns. Of course, we already knew that people age at different rates because we see some people fit and healthy into the 10th decade whereas some are not so lucky and seem to get the diseases of old age as early as their 5th decade. But to have a simple test to confirm this and allow people to assess the age their cells are acting compared to their chronological age is an incredible breakthrough.

What is exciting is that your biological age does not need to be your destiny and can be changed. If you have turned 50 and your DNA methylation is at a level that is usually seen with someone in their 70s then by making lifestyle changes like exercise and diet and taking new supplements you can bring your biological age into line with your chronological age. And perhaps even more exciting is that if your results are similar you can take the same actions to slow down your biological aging. It is entirely possible in your chronological 50s or 60s that you could celebrate your 40th or 30th decade again! And it is available to everyone, today, right now with simple actions.

Moving from luck to strategy in aging
For the first time in human history we are about to take the luck out of getting old with health and vitality and make healthy aging with an extended healthspan accessible to us all. In my book, “Harnessing the Nine Hallmarks of Aging,” I have distilled the very latest in research and created a lifelong healthy aging plan for people who want to age better and arrive at a more mature age with more health and vitality than any previous generation of humans have obtained. I describe specific strategies for those who are in their 30s, 40s, 50s and beyond and share breakthroughs in our understanding of what molecules and supplements can impact and slow the aging process.

For example, molecules like Hobamine (2-HOBA)⁹, an extract from Himalayan Tartary Buckwheat, has recently been isolated and shows incredible potential to slow the aging process by protecting our delicate DNA and other cellular components and machinery from the damage associated with oxidative stress throughout our lifetime. Also, NAD, nicotinamide adenine dinucleotide, is an important co-enzyme that fuels our mitochondria and our cellular repair and maintenance mechanisms. NAD levels decline in our cells as we age, so by restoring this vital co-enzyme via supplements like NMN¹⁰ (nicotinamide mononucleotide) researchers have seen changes in our cells that are associated with levels of health seen in cells that are considerably younger.

Fisetin¹¹, a compound derived from strawberries and other fruits, has the ability to reduce the burden of senescent cells in the body. Senescent cells are cells that have reached the end of their useful life. In younger animals these cells are removed by our immune system, however as we get older our immune system is not as effective in clearing these cells out. The very signals senescent cells send out to communicate they need to be removed from our bodies then start to accumulate leading to an increasingly inflammatory state that has a significant effect on the health of the rest of the cells in our body. Recently, researchers have discovered that by taking fisetin you can help your body remove these unwelcomed zombie-like cells and by doing so you can experience major health benefits. In mouse models, fisetin can increase lifespan by as much as 36%. In another study¹², older mice pretreated with fisetin and then exposed to a similar virus to COVID respond to the virus in a way that is more like younger mice suggesting that the reason older humans are so affected by COVID is related to the burden of senescent cells in their bodies. The Mayo Clinic now has clinical research underway to see if the benefit the mice experienced will be replicated in humans¹³.

In the future, there will be significant advances in our ability to slow the aging process beyond what we have available to us today. For now however, adopting the strategies outlined in “Harnessing the Nine Hallmarks of Aging” will help you slow the speed of aging that your cells experience, and with this you are taking affirmative action to delay the diseases associated with old age. The sooner you start the better shape your cells will be in and this will be reflected in how you feel, how you look and increase your healthspan – the amount of time you spend in your body while experiencing amazing health.

References

1. This Tiny Animal Can Live an Estimated 1,400 Years – Scientific American
2. Science of the immortal jellyfish, Earth’s longest living animal – Science Focus
3. A living bdelloid rotifer from 24,000-year-old Arctic permafrost – ScienceDirect
4. Longitudinal analysis of blood markers reveals progressive loss of resilience and predicts human lifespan limit | Nature Communications
5. House mouse (Mus musculus) longevity, ageing, and life history – senescence.info
6. Naked mole rat may hold the secret to long life – phys.org
7. The Hallmarks of Aging: Cell
8. Epigenetic clock – Wikipedia
9. 2-hydroxybenzylamine – Search Results – PubMed
10. Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice – nih.gov
11. Fisetin is a senotherapeutic that extends health and lifespan – PubMed
12. Senolytics reduce coronavirus-related mortality in old mice | Science
13. COVID-FISETIN: Pilot in SARS-CoV-2 of Fisetin to Alleviate Dysfunction and Inflammation – ClinicalTrials.gov

The post More Than Good Genes: Breakthrough Science Shows Us How To Slow Down The Aging Process appeared first on Total Health Magazine.

The term essential fatty acid refers to a fatty acid, which the body cannot manufacture and must obtain from dietary sources. These essential fatty acids were originally designated as Vitamin F, until it was realized that they must be classified with the fats.³ There are two fatty acids designated as essential fatty acids: linoleic acid and alphalinolenic acid. This does not mean that the other 15 or so fatty acids found in the omega 3, 6 and 9 groups aren’t important, just that a healthy body can manufacture them as long as it gets enough linoleic acid and alpha-linolenic acid. Nevertheless, research demonstrates that there are health benefits to be had by obtaining some of the other non-essential fatty acids directly; more on this later. Now let’s discuss the roles of essential fatty acids (EFAs) in the body, as well as sources of EFAs.

Roles and sources of essential fatty acids
The body uses essential fatty acids (EFAs) for the formation of healthy cell membranes, the proper development and functioning of the brain and nervous system, and for the production of hormone-like substances called eicosanoids (thromboxanes, leukotrienes, prostaglandins). These chemicals regulate numerous body functions including blood pressure, blood viscosity, vasoconstriction, immune and inflammatory responses.⁴

Dietary sources of the omega 6 fatty acids include some leafy vegetables, seeds nuts, grains, vegetable oils and meats. Dietary sources of the omega 3 fatty acids include some vegetable oils, nuts and seeds, shellfish and fish.⁵ Dietary supplement sources of essential fatty acids and nonessential fatty acids include Evening Primrose oil, Borage oil, Flax seed oil and Fish oils (marine lipid concentrate). Now let’s take a look at some of these individual dietary supplement sources of essential fatty acids, and the benefits they have to offer.

Evening Primrose & Borage Oils: Sources of GLA The oils from the Evening Primrose plant and Borage seed are rich in the omega 6 fatty acid, gamma linolenic acid (GLA); as well as EFAs. Although fatty acids are found in significant quantities in a variety of plants, GLA is only found in a few. GLA is a precursor to various natural chemicals found in the body. Among these are prostaglandins, a type of short-term hormone-like substances, which play a variety of roles in the body. Published research on these sources of GLA have demonstrated them to be useful in PMS^{6,7,8,9,10,11}, pregnancy and lactation^12,13, inflammatory conditions^14,15, rheumatoid arthritis^16,17,18, skin conditions^{19,20,21,22,23,24,25,26,27,28,29,20,32,32,33,34}, stress and performance^35,36, as well as migraine headaches.³⁷ Furthermore, the unique balance of GLA to EFAs in any one of these sources may have a distinct benefit over another source depending on the condition in question. For more detailed information on EPO and BO, read the Intelligent Supplementation article, “GLA: Gamma Linolenic Acid from Evening Primrose & Borage Oils.”

Fish Oils: Sources of EPA/DHA Omega 3 fatty acids
Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are omega 3 fatty acids (O3FA). O3FA supplements are mostly derived from the oils of cold water species of fish like salmon, sardines, herring, and mackerel. There are many therapeutic applications for O3FA, primarily due to its cardiovascular-enhancing and anti-inflammatory benefits. Research has shown that O3FA cardiovascular benefits include reducing the risk of atherosclerosis^{38,39,40,41,42,43,44}, modifying cholesterol levels (i.e., increasing “good” HDL cholesterol, while decreasing “bad” LDL cholesterol) and decreasing triglycerides^{45,46,47,48,49}, and decreasing high blood pressure.60 O3FA have also been shown to block the production of certain inflammatory chemicals in our body. Consequently, studies have demonstrated the ability of O3FA to reduce inflammation in such disorders as rheumatoid arthritis^51,52,53,54, asthma^55,56,57,58, colitis^{59,60,61,62,63}, Crohn’s disease^64,65,66, and Lupus^67,68,69. In addition, O3FA have shown to reduce the symptoms of other disorders including angina^70,71, migraine headaches^72,73,74,75, psoriasis^{76,77,78,79,80}, and tinnitus.^81,82 For more detailed information on O3FA, read the Intelligent Supplementation article “Omega 3 Fatty Acids.”

Flax Seed Oils: Sources of Omega 3, 6 & 9 fatty acids

Flax seed naturally contain a complex of different categories of fatty acids, including alpha-linolenic acid (omega-3), linoleic acid (omega-6), and oleic acid (omega-9). Much of Flax seed’s benefits are a function of its alpha linolenic acid (ALA) content, and the fact that ALA can be converted by the body into EPA—the same omega-3 found in fish oil. As a matter of fact, research has found that supplementation with Flax seed oil can effectively increase EPA concentrations in tissues.⁸³ Lignans, also found in Flax seed, account for various benefits offered by this plant. Studies involving Flax seed have been conducted on its anti-inflammatory properties84, its antilupus properties⁸⁵, and its cardiovascular enhancing properties.^{86,87,88,89,90,91}

Just a quick note to mention that the omega 9 fatty acid, oleic acid, has been shown in research to lower heart attack risk and arteriosclerosis92, and aids in the prevention of breast cancer.⁹³

Conclusion
In addition to the two essential fatty acids, there are other fatty acids whose consumption may have benefits for human health. Both the essential and non-essential fatty acids can be obtained from dietary supplement sources including Evening Primrose oil, Borage oil, Flax seed oil and Fish oils (marine lipid concentrate). Each of these sources has their own potential advantages. Perhaps a combination of all of them may yield the broadest spectrum of both essential and nonessential fatty acids.

References:

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3. Answers to Frequently Asked Questions. USDA Nutrient Data Laboratory, Agricultural Research Service. Last modified July 22, 2005. Accessed on August 18, 2005
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10. Casper R. A double-blind trial of evening primrose oil in premenstrual syndrome 1987; September, 2nd International Symposium on PMS, Kiawah Island.
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17. Rothman D, DeLuca P, Zurier RB, Semin Arthritis Rheum 1995; 25(2):87–96.
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27. Businco L, et al, J Allergy Clin Immunol 1993; 91(6):1134–9.
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43. Hu FB, Bronner L, Willett WC, Stampfer MJ, Rexrode KM, Albert CM, et al. Fish and omega-3 fatty acid intake and risk of coronary heart disease in women. JAMA 2002; 287:1815–21.
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45. Santos MJ, Lopez-Jurado M, Llopis J, et al. Influence of dietary supplementation with fish on plasma total cholesterol and lipoprotein cholesterol fractions in patients with coronary heart disease. J Nutr Med 1992; 3:107–15.
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68. Walton AJE, et al, Ann Rheum Dis 1991; 50:463–66.
69. Westberg G, Tarkowski A, Scand J Rheumatology 1990; 19:137–43.
70. Saynor R, Verel D, Gillott T, Atheroscl 1984;50:3–10.
71. Mehta JL, et al, Am J Med 1988; 84:45–52.
72. McCarren T, et al, Am J Clin Nutr 1985;41(4):874 [abstr].
73. Glueck CJ, et al, Am J Clin Nutr 1986;43(4):710 [abstr].
74. Gibson RA, Australian and New Zealand Journal of Medicine 1988; 18(5):713–22.
75. McCarty MF, Medical hypotheses (1996) 47(6):461–6.
76. Bittiner SB, et al, Lancet 1988; i:378–80.
77. Kojima T, et al, Dermatologica 1991; 182:225–30.
78. Kojima T, et al, J Am Acad Dermatol 1989;21:150–51.
79. Dewsbury CE, Graham P, Darley CR, Br J Dermatol 1989; 120:581–84.
80. Ashley JM, et al, J Am Acad Dermatol 1988; 19:76–82.
81. Rudin, D., Med Hypotheses 1980; 6(4): 427–30.
82. Rudin, D., Biol Psychiatry 1981; 16(9): 837–50.
83. Mantzioris E, et al, Am J Clin Nutr 1994; 59(6):1304–9.
84. James MJ, Gibson RA, Cleland LG, Am J Clin Nutr 2000; 71(1Suppl):343S–8S.
85. Clark WF, et al, Kidney Int 1995; 48:475–80.
86. Bierenbaum ML, Reichstein R, Watkins TR, Journal of the American College of Nutrition 1993; 12(5):501–4.
87. Harris WS, Am J Clin Nutr 1997; 65(5 Suppl):1645S.
88. Cunnane SC, et al, Am J Clin Nutr 1995 ; 61(1):62–8.
89. Cunnane SC, et al, Br J Nutr 1993 ; 69(2):443–53.
90. Prasad K, Atherosclerosis 1997; 132(1):69–76.
91. Nestel PJ, et al, Arterioscler Thromb Vasc Biol 1997; 17(6):1163–70.
92. Rotella P. Healthy Fats–Essential Fatty Acids. Posted 13 April 2002, Last updated 22 October 2004. Accessed August 19, 2005 from http://goodfats.pamrotella.com.
93. Menendez JA, Vellon L, Colomer R, Lupu R. Annals of Oncology 2005; 16(3):359–71.

The post Essential & Nonessential Fatty Acids appeared first on Total Health Magazine.

FOUR KEY FACTORS TO CONSIDER

1. Telomeres—These are little caps at the end of our chromosomes that help to keep our DNA contained when cells divide in the replacement process. With each replacement (50–70) these telomeres get shorter until replication is stopped and we die. These telomeres get shorter if we do not eat a perfect diet, experience too much stress, do not get enough sleep, are exposed to toxins or do not get enough physical activity.
2. Oxidation—Our cells oxidize and deteriorate if we consume too much sugar, alcohol, saturated fat or toxins. This damage occurs to our DNA, the mitochondria in our cells, as well as the proteins and lipid fats needed for healthy aging. Antioxidants such as vitamin C and vitamin E can neutralize these oxidants and preserve the integrity of our cells for excessive damage.
3. Glycation—Sometimes sugar and proteins do not interact properly causing advanced glycation end products (AGES). A good example is when red meat is cooked at high temperature and the molecules are disturbed and restructured. Radiation is another example of this happening. These altered molecules can begin the process of disease that accelerates aging.
4. Cellular malnutrition—Every cell needs a high level of nutrients to do the jobs they are programmed to do like make the heart, brain, liver, lungs and kidneys function properly. Without excellent nutrition, cells deteriorate in five distinct stages from being stressed, weakened, dysfunctional, mutated and finally diseased. This cellular deterioration process also causes premature aging and chronic disease.

Improvements Against Premature Aging

• Reduce sources of stress
• Practice meditation or yoga
• Get regular exercise
• Get enough sleep ( 7–8 hours)
• Reduce toxins in your life
• Eat more organic vegetables and fruits, along with seeds, nuts, omega fish, olive and coconut oil
• Drink spring water (no chlorine or fluoride)
• Get good health tests from a Functional Doctor
• Consume quality nutritional supplements

Nutritional Supplements To Prevent Premature Aging ( Slow Telomere Erosion )

• Vitamin A
• Vitamin B complex*
• Omega 3 fats
• Astaxanthin
• Zinc
• Vitamin D3
• Vitamin E
• Curcumin
• Green Tea
• Iron
• Vitamin C
• CoEnzyme Q10
• Probiotics
• Magnesium
• Polyphenols

These are general strategies and will need to be adjusted based on specific factors such as age, sex, general health, metabolism (there are five types), genetics and income. We all can only do the best that we can do given our personal circumstances. However, there is no excuse for not paying attention to the scientific facts that are included in this article. If you want to enjoy a healthier and longer life, then it is up to you do the best that you can do to make sure that happens.

Delaying the Aging Process One Meal at a Time
Genes play an important role in how long we live, but nutritional scientist feel there are other factors that are even more important, and about 80 percent of them are within our control. Nutrition is the most important factor along with a few other important health considerations. Here are my top ten.

1. Organic food—Organic food has higher levels of nutrients and lower levels of pesticides, which increases the vitamins and minerals important to brain health. (Magnesium, vitamin A and C)
2. Nutritional density—Whole foods such as vegetables, fruits, nuts, seeds, omega fish and oils such as olive and coconut oil are the best. Avoid red meat, dairy, sugar, alcohol or processed foods.
3. Chewing—Chew most foods 20–30 times or you can lose up to 50 percent of the nutrients because the food particles were too large or amylase enzymes were not released sufficiently in the saliva.
4. Small meals—Eating three meals and two snacks each day will allow for better digestion and absorption of the food. It will also provide a better distribution of the calories to help control weight.
5. Enzymes, acid, and bacteria—By the age of 50 we are producing 50 percent less digestive enzymes, stomach acid and intestinal bacteria. Eat raw foods and take digestive supplements to help.
6. Nutritional supplements—Food has fewer nutrients than it did 50 years ago according to the USDA. This is caused by depleted soil, minerals not added, processing, and long transit. There are over 15,000 scientific studies supporting the need for supplemental vitamins, minerals, and healthy oils. Doctors like Daniel Amen, Mark Hyman, and Joseph Mercola can offer guidance online.
7. Toxins—The level of toxins in the air, water, and our food has increased dramatically over the years. Toxins cause our cells to age prematurely and become diseased. Avoid tap water, which contains chlorine and fluoride; use pure spring water instead. Use an air purifier at home and at work. Exercise regularly, take a sauna and use detox programs like the one by Brenda Watson.
8. Diagnostic tests—Conventional blood tests do not diagnose most disease until it is already well developed. Find a doctor who specializes in holistic or functional medicine to get the right tests.
9. Sleep—Our bodies need seven to nine hours of sleep each night in order to properly detoxify and balance our systems, such as the acid/alkaline balance. The hours before midnight are very important as is a diet with enough amino acids, B vitamins, calcium, and magnesium.
10. Stress—is implicated in over 80 percent of all illness and happens 30 to 40 times every day. Avoid the stress you can avoid and use meditation, yoga and deep breathing to calm you down.

A brilliant nutritional scientist, Bruce Ames, has shown that nutrients we consume are utilized on a priority basis with reproduction and germ treatment first and chronic disease and longevity last. This is why we are facing a significant health crisis in this country.

• The National Cancer Institute studied over 14,000 people aged 2 to 80 and could not find one person with a truly healthy diet. In fact, most were deficient in 11 out of 14 nutritional categories.
• Over 60 percent of adults have one or more chronic illnesses. This is up from 10 percent about 60 years ago. This is why healthcare costs are going through the roof in the United States.
• The lifespan of the average person just went down for the first time in decades and it is going to get much worse. Children born after the year 2000 will face a 40 to 50 percent risk of diabetes, which is up over 400 percent in the past 50 years.

The odds of getting healthier and growing older without disease are not good unless you get serious about it and take the steps mentioned above.

The post Changing Your Age Equation appeared first on Total Health Magazine.

• Poor nutrition
• High toxin levels
• Poor sleep
• High stress levels
• Genetic predispositions
• Under or over exercising

Conventional medicine typically uses drugs and surgery to address these health challenges, however, these are usually not sustainable strategies. Treating symptoms and managing disease is not as valuable as preventing and reversing disease.

NAD (nicotinamide adenine dinucleotide) is a form of vitamin B, acting as an enzyme that has been proven to be a key nutrient in preventing and reversing the cellular damage previously mentioned. This diagram depicts the five stages of cellular deterioration that could be delayed with the use of NAD.

Markers of Cellular Deterioration
As cells continue to experience these assaults on our cellular health, our bodies begin to produce recognizable markers of this deterioration, including:

• Inflammation
• Oxidative stress
• Metabolic dysfunction
• Symptoms of deficiency
• DNA damage
• Biochemical imbalances
• Disease (heart disease, diabetes, cancer, etc.)

Early Warning Health Assessment
Cell replacement and survival become seriously compromised if these cellular reactions are not caught soon enough. Some good diagnostic tools that can provide some early warning protection include:

• The glucose challenge test
• Thermography
• C-reactive protein
• Homocysteine
• Galectin 3
• Vitamin D3 levels
• Heavy metals levels
• Omega 3/6 levels
• NA/NADH ratio
• Fibrinogen

By using these early warning health assessment tools, it has been proven that natural/functional medicine doctors can prevent and reverse over 80 percent of all chronic illness, and the formula for this prevention and reversal process is usually the same in each case.

1. Identify and remove toxins in the body.
2. Adopt a Mediterranean style diet.
3. Use moderate exercise, including aerobic, resistance and flexibility.
4. Use quality nutritional supplements as needed.
5. Practice meditation, yoga and other positive thought practices. Reduce stress as much as possible.
6. Get good restorative sleep every night.

The evidence-based science behind these natural approaches is indisputable and will eventually be adopted by everyone once the profit-driven health care system is dramatically changed. We need a health and prevention system instead of a disease management profit-based system.

NAD Major Cell Protector

NAD is now beginning to assume its role as the next superstar in this strategy to improve cellular health in some very serious ways. Here are the primary improvement categories for cellular health improvement identified in current NAD research.

• Reduced levels of cellular inflammation (NF-KB).
• Reduced levels of free radicals (oxidative stress).
• Improved metabolic homeostasis (biochemical balancing).
• Reduced cell cycle disturbances via ADP-ribose, polymerase (PA R P-1) and sirtuins (Sirt-1-7).
• Repair of DNA damage in cell nucleus.
• Improvement in cell mitochondria function (energy).

The cell cycle process controls cell replacement and cellular death. If any of the key change junctures are negatively influenced by toxins, poor nutrition or stress of some kind, then this cycle could be disrupted, leading to the development of inferior cells, mutated cells or even cell death. NAD has the ability to correct these disturbances and even fix mutated DNA if it can be delivered to the cells before permanent mutation can occur.

As We Age
In addition to the impact of poor nutrition, toxins, and stress, there are also natural genetic and biochemical changes that happen as part of “normal aging.” Cellular replacement time declines, enzyme, probiotic and antioxidant levels decline, and, levels of NAD decline. We can address most of these cellular aging factors with better diet, detoxification, stress reduction and supplementation with key enzymes, probiotics, and other nutritional supplements, include NAD. This aging process, as related to the presence of NAD, looks something like this:

1. NAD declines with age — The DNA in our cells becomes damaged due to assaults by free radicals. This increases the need for NAD, because it is a key element of the DNA repair process.

2. NAD/NADH ratio — This decline in NAD can change the ratio of NAD/NADH, which causes disruption to the basic cellular processes it facilitates.

3. Early cellular changes — Low NAD leads to decreased mitochondrial oxidation and insufficient ATP production. Low energy.

4. Low energy consequences — Insufficient cellular energy impedes cellular function, including DNA maintenance and repair.

5. Mitochondrial communication—Reduced mitochondrial communication impedes cellular defense mechanisms, such as immune function as well as increased vulnerability for microbial illnesses, genetic predisposition and biochemical imbalances. (Diabetes, heart disease, etc.)

Increasing NAD levels
The very first step in this effort to increase NAD levels is to get the NAD/NADH blood test. This will establish the existing levels of NAD homeostasis. Then, if levels are low or out of balance, the following steps can be taken:

• Eat these foods high in NAD—Green vegetables, chicken, fish, crimini mushrooms, yeast, beer and dairy products (preferably goat products).
• Take a good NAD supplement—One of the earliest products was developed by Life Extension Foundation, which contains the patented ingredient, NIAGENTM.

The probable outcomes of increasing NAD levels:

• Reduce inflammation
• DNA repair
• Increased energy
• Improved immune function
• Genome integrity
• Damaged cell replacement
• Reduced oxidative stress
• Reduced aging stress
• Decreased susceptibility to cancer.
• Resolution of many heart disease challenges.
• Reduced blood pressure due to improved arterial flexibility.
• Improved function for early stage organ compromise.
• Improved cellular preformation related to addiction issues.
• Possible improvement in various brain related challenges, such as depression, anxiety and dementia.

Summary
While we should be cautious about using the term “miracle cure,” it is obvious that NAD plays a crucial role in our cellular health. We know that levels of NAD decline by as much as 50 percent between the ages of 40 and 50. We also know that this decline has a potentially negative impact on every one of our 60 trillion cells.

• Free radicals cause damage to our DNA, which is a proven cause of disease, such as diabetes, heart disease, cancer and many brain-related illnesses.
• NAD can protect our cells from the damage and, in some cases, can even reverse some of this damage. The science behind this is growing every day.
• To achieve optimal health, we need to do many things, including taking quality nutritional supplements. There is no science to dispute this fact.
• NAD should definitely be one of those supplements, and adding it is a wise decision.

The post NAD The Superstar for Cellular Healing appeared first on Total Health Magazine.

Genes represent a genetic predisposition to a given disease, which means that it is still within our power to prevent or activate them based on controllable factors.

Controllable Factors
Many environmental factors are controllable, such as what we eat and drink, and other lifestyle factors, such as alcohol or tobacco consumption. Toxins also have a major influence, but often we cannot avoid them, as is the case with most electromagnetic radiation. The following list illustrates most of the factors that can influence genetic expression.

• Nutrition
• Oxidative stress
• Inflammation
• Body type
• Gut health
• Pathogens
• Radiation
• Chemical contaminants
• Medical interventions
• Pharmaceuticals
• Psychological stress
• Social/economic status
• Climate
• Urban/rural influences

Changing our Genes

It is also possible to alter our genetic expressions for future generations. If a parent experiences a traumatic environment, such as serious radiation exposure, tobacco consumption, nutritional deficiencies or disease expression (i.e. Type 2 diabetes) before child bearing, these influences can be added to that person’s genetic expression.

The genotype is what we receive at birth from our parents and the phenotype is everything that happens to influence our genes from the day we are born. And, as was just stated, our phenotype can help to influence our children’s genotype, if these influences occur before a child is born.

For example:

• The children of Holocaust survivors are often at higher risk of post-traumatic stress disorder, anxiety and depression.
• Women who undergo famine before conception have been shown to experience disorders such as, hypertension, schizophrenia, nervous system disorders, cardiovascular disease and obesity in offspring.
• The survivors of atomic bomb explosions in Hiroshima and Nagasaki have been shown to produce children with an increased risk of cancer.

And emerging research indicates that these newly developed genetic influences can persist into the future, in as many as fourteen generations.

The Good News For Our Genes
While there are many negative influences that can influence our genetic expression, there are also many positive influences that can negate or balance these expressions. Some well-known positive genetic influences include:

• The Mediterranean Diet has been shown to reduce the risk of chronic illnesses such as heart disease, cancer, Type 2 diabetes and high blood pressure.
• Exercise to help remove toxins and enhance metabolic processes.
• Mindfulness that can help produce biochemicals to stop disease expressions, enhance immune function and improve cardiovascular health.
• Sulforaphane found in cruciferous vegetables helps improve gene expression.
• Resveratrol from red grapes has proven benefits for the heart and much more.
• Genistein found in soy can help modify cancer gene expressions.
• Diallyl sulphide from garlic improves overall immune function.
• Curcumin from turmeric is a major anti-cancer and anti-inflammation spice with strong and positive genetic expression capabilities.
• Betaine from beets has strong metabolic influences.
• Vitamin D from fish oil is probably the strongest proven nutrient for the reduction of negative genetic expressions, especially cancer.

These and other positive influences have been proven to modify genetic expression in a very significant positive way. For example, high levels of vitamin D3 can reduce the risk of breast cancer by 77 percent and prostate cancer by 84 percent.

Early Interventions Are Possible
And now, using the power of artificial intelligence based on functional medicine, it is possible to use a saliva sample to find out the negative genetic expressions you now have. Then a special database/software program can help identify the specific interventions, mostly nutritional, that can be used to minimize these negative influences. This powerful epigenetic tool could be the most powerful influence identified to date for the prevention of chronic illness in future generations.

The post How Do Genes Influence Our Health? appeared first on Total Health Magazine.

• Kidneys can be diseased by 90 percent before tests ever indicate a problem.
• Liver disease is often detected after the liver is 70 percent diseased.
• Heart disease has often been developing 20 years before traditional tests reveal a problem.
• Breast cancer is usually detected with a mammogram, which is eight to ten years before cancer begins to develop.
• Diabetes tests include the AIC test, which often detects a problem five to ten years after it could have been detected.
• Alzheimer’s cannot be detected, by conventional medicine, until there is a beginning of loss in cognitive function.
• Parkinson’s Disease is only detected when a slight trembling occurs in one finger of one hand. By then about 80 percent of all dopamine receptors in the brain have died or been seriously damaged.

Disease usually happens in five distinct stages:

1. Stressed cells happen when there is poor nutrition,high toxin levels, high stress levels and genetic or biochemical deficiencies.
2. Weakened cells occur when cells have been stressed too long, and cells lose their energy level.
3. Dysfunctional cells are the third stage of deterioration when cells begin to experienced functional challenges. This is when most traditional tests detect a problem, such as high blood pressure, high glucose or chest pain known as angina.
4. Mutated cells occur when the nucleus of the cell becomes damaged and can no longer produce a healthy replacement cell.
5. Diseased cells happen when the cell cannot function and begins to damage other neighboring cells.

The post The Early Detection of Chronic Disease appeared first on Total Health Magazine.

Are many or even most of the health challenges in modern Western societies—high blood pressure, high blood sugar, high cholesterol levels, cardiovascular disease in general, weight problems, etc.—related? There is a good case to be made that they are.

At the core of Syndrome X, now much more commonly known as the metabolic syndrome, are dysregulations and dysfunctions involving glucose and insulin. These manifest as central obesity (excessive fat around the belly), high blood pressure and blood fat disorders—especially hypertriglyceridemia and low levels of HDL cholesterol. In addition to participating in the development of many facets of the metabolic syndrome, impairment in insulin sensitivity also appears to be involved in the aging process by promoting inflammation, endothelial dysfunction (problems with the blood vessels), the production of advanced glycation end products (AGE) and oxidative stress. Downstream consequences of these dysfunctions include cardiovascular disease and cancer. These issues were discussed approximately one year ago in this magazine under the heading “Is the Metabolic Syndrome a Consequence of Aging?” (May 2017) Nonalcoholic fatty liver disease was not originally included in metabolic syndrome manifestations. However, over the past decade medical thinking by almost all parties regarding the relationship of these conditions has moved strongly towards viewing them as linked in some way. From 15 to 33 percent of the worldwide population is estimated to suffer from non-alcoholic fatty liver disease.

As noted in the earlier article, major questions remain regarding the early appearance of the metabolic syndrome. Western medicine, unlike, for instance, traditional Chinese and Indian medicine, tends to pursue and treat the various arms of the metabolic syndrome as distinct clinical entities. Much of the research on the syndrome within allopathic medicine over the past three decades has been aimed at arguing against this separation. Questions regarding the liver and metabolic syndrome involve similar issues. According to some authorities, non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. However, others believe NAFLD is a distinct entity that actually initiates the metabolic syndrome. The choice as to which comes first, the metabolic syndrome or NAFLD, if indeed they are distinct, helps to determine how each can be prevented and treated.

Early Signs of the Metabolic Syndrome

Most clinicians consider a level of circulating glucose under fasting conditions in the range of 100–125 mg/dl to be prediabetic, but agreement beyond this is hard to come by. Normal levels of blood glucose and circulating insulin, meaning levels that do not lead to components of the metabolic syndrome, remain in dispute. Nevertheless, evidence suggests that surprisingly “normal” fasting blood glucose levels still have consequences.

Circulating glucose within levels generally accepted as normal can influence brain function in an unfavorable manner. Similarly, increasing hemoglobin A1C (HbAlC) and insulin levels even in the non-diabetic range can affect blood pressure adversely. Such observations lead to suspicions that minor insulin resistance predicts the early onset of many disturbed health parameters involved in the metabolic syndrome. Recently, Harry G. Preuss and co-authors, of whom I am one, addressed just such questions in “General Lack of Correlations between Age and Signs of the Metabolic Syndrome in Subjects with Non-diabetic Fasting Glucose Values.”¹

Based on our study, the health data were significantly better with fasting glucose levels in the range of 67–86 mg/dL than at 98–125 mg/dL. Across a wide range of variables lower definitely was better leading to the conclusion that decreasing insulin resistance and maintaining fasting glucose levels at the low end of the normal range is highly desirable. Advancing years did not appear to be a factor leading to the metabolic syndrome. In terms of the present topic, using the data at hand, advancing age per se also did not seem to affect liver health.

Non-Alcoholic Fatty Liver Disease and the Metabolic Syndrome in Non-Diabetics
If aging is not a primary factor in the appearance of the metabolic syndrome, yet NAFLD and the metabolic syndrome are linked, some other cause or causes are at work. The usual list of suspects can be found in the typical elements examined to determine diagnosis.

Aside from ruling out an elevated consumption of alcohol, a verdict of NAFLD primarily is based on discovering excess liver fat accumulation along with raised circulating aminotransferase levels generally involving ALT more than AST. For clarity, the latter are “two important transaminase enzymes…aspartate transaminase (AST), also known as serum glutamic oxaloacetic transaminase (SGOT); and alanine transaminase (ALT), also called alanine aminotransferase (ALAT) or serum glutamatepyruvate transaminase (SGPT)… [Transaminases] are important in the synthesis of amino acids, which form proteins.”² Liver health and function is evaluated by, among other markers, the levels of ALT, ALS and their ratio. Whenever a patient gets blood drawn for basic blood panel tests, ALT and ALS are checked.

Alanine aminotransferase (ALT) found persistently to be elevated often is viewed as indicating the presence of NAFLD. More generally, an elevated circulating concentration of ALT is recognized to be a fairly specific sign for liver injury. In considering the “normal” range of ALT (<40 U/L) for cardiovascular disease in general, unfortunately the normal range does not represent a cut-off below which one is safe, but, instead, a point of a continuum of risk.³

Starting with a subject population that is non-diabetic and without any of the normal signs of liver dysfunction, the question, again, is whether NAFLD is a component of the metabolic syndrome or, instead, is an independent disorder that precedes and actually initiates the onset of the syndrome. The answer to this question has important implications for the treatment of both conditions. On the one hand, if the metabolic syndrome, meaning primarily insulin resistance, is the central issue and NAFLD is really just a component of the syndrome, even should there be feedback once NAFLD is established, then the metabolic syndrome is tackled first to prevent or treat its manifestations in the liver. On the other hand, if the hepatic condition is first in time and in causality, treatment starts with the liver.

Treating NAFLD: The Liver Or Insulin Resistance
A major reason for looking closely at the relationship between the metabolic syndrome and NAFLD is that treating the latter with approaches aimed specifically at the liver has yielded underwhelming levels of success. The single most successful standalone natural ingredient probably is mixed tocotrienols taken 200 mg twice per day for a year.⁴ Overall, 13 of 26 subjects (50 percent) became NAFLD-negative. In those with a mild form, there was a 38 percent decrease in the number of subjects with active disease at the end of the study, indicating that improvement was linked to the severity of the condition. Somewhat less impressive was silybin (an active component of milk thistle extract) combined with phosphatidylcholine and vitamin E acetate (á-tocopherol), again, taken for twelve months. Still, the formula significantly improved liver conditions associated with NAFLD (steatosis, lobular inflammation, ballooning, and fibrosis) and the overall NAFLD Activity Score.⁵ Interestingly, in another trial the results with milk thistle and vitamin E were much improved in patients who followed a low calorie diet with weight loss.⁶

Findings of this sort strengthen the argument that NAFLD is an aspect of the metabolic syndrome and not its cause. A number of studies have demonstrated that hepatic insulin resistance likely is the chief culprit.⁷ For instance, the accumulation of triglycerides in the liver is a cause of the condition. Technically, hyperinsulinemia promotes the upregulation of genes that promote de novo lipogenesis (biosynthesis of fat) in the liver.^8,9

Given evidence that de novo lipogenesis, which primarily is induced by high insulin levels and refined carbohydrates, is an important agent in the development of liver dysfunction, it can come as no surprise that an inhibitor of this process, (–)-hydroxycitric acid (HCA), improves liver function in experimentally-induced nonalcoholic steatohepatitis (NASH), a component of NAFLD. In animal experiments, both liver fibrosis and markers of liver function were improved under experimental conditions with ingestion of HCA.^10,11 It should be noted that, experimentally, liver dysfunction is closely associated with the intake of rapidly absorbed carbohydrates, but not necessarily carbohydrate consumption itself.¹² In humans, short-term fructose consumption in either isocaloric exchange or in hypercaloric supplementation promotes the development of hepatic insulin resistance in non-diabetic adults without affecting peripheral or muscle insulin sensitivity.¹³ Indeed, at this point there is little doubt but that fructose consumption in excess is a primary driver of the synthesis of triglycerides and other perturbations of the handling of fats by the liver leading to fatty liver disease.¹⁴ Fructose appears to induce both NAFLD and metabolic syndrome through related mechanisms.¹⁵ A steadily growing body of evidence supports the position that medium and long-term excess ingestion of fructose and rapidly absorbed carbohydrates progressively distort the handling of glucose and insulin not just in the liver, but also in the muscles and other lean tissues.

Back to the Chicken and Egg Question
So, what do we have so far? Evidence from animal models and human experience indicates that certainly one or more of the drivers of liver dysfunction—fructose and rapidly absorbed carbohydrates—act initially on the liver to cause insulin resistance. Liver insulin resistance subsequently makes general control of blood sugar levels more difficult and causes the body to release more insulin and/or insulin in greater amounts at a given time to regulate blood sugar, an action with particularly unfortunate consequences after meals. Over time, elevated glucose and insulin levels originally caused by the liver lead to insulin resistance in the muscles and other lean tissues, tissues that account for approximately 70 percent of all glucose clearance in the body.

In addition, there is a feedback loop between the liver and peripheral lean tissues that involves the metabolism of fats for energy and storage. Initially, circulating elevated levels of blood glucose result from hepatic insulin resistance whereas increased circulating free fatty acid concentrations are a primary expression of peripheral insulin resistance.¹⁶ Insulin, of course, controls the clearance and energy metabolism of both fuel sources; as a storage hormone, insulin in excess directly impedes the use of fats for energy, hence contributes to elevations in blood free fatty acids and triglycerides. The effects are bidirectional: insulin resistance leads to fat accumulation and fat accumulation amplifies insulin resistance.

This line of argument and supporting evidence suggest that the metabolic syndrome and NAFLD generally are linked from the start and take form largely concurrently. Forthcoming work by the team of Harry Preuss et al, indicates exactly this. ALT and the ratio of AST/ALT correlate significantly with fasting blood glucose in non-diabetics indicating that these markers of liver health move largely in unison with changes in insulin sensitivity. Insulin resistance drives both the metabolic syndrome and NAFLD.

What Is To Be Done?
Key to improving liver health are diet and exercise habits. This fact showed up in the treatment option mentioned above which combined milk thistle with vitamin E—results were much better in the subjects on a low calorie diet. Nutrients such as tocotrienols, milk thistle, quercetin and other liver supports and detoxifiers only marginally address the primary issues. These primary issues include:

• Consumption of rapidly absorbed carbohydrate sources, especially fructose, as discussed in the foregoing text
• Ingestion of foods that lead to elevated insulin release when eaten with refined carbohydrates; these include red meat and branched-chain amino acid sources¹⁷
• Reduced metabolism of fats for energy; certain food combinations, such as fats eaten with rapidly absorbed carbohydrates, severely interfere with the utilization of consumed fats for energy with negative implications for both liver and muscle insulin sensitivity
• Reliance on ultra-processed foods, meaning a preponderance of the foods now eaten in the US and many European nations ^18,19,20 (see “Calories Don’t Add Up“
• A lack of regular exercise: 15–30 minutes twice per day is recommended

For success, the right tool must be applied for the proper purpose. Although it is true that the environment increasingly is polluted with various toxins, NAFLD predominantly is a result of the foregoing issues. Correspondingly, corrective nutrients and herbs for NAFLD, just as with the metabolic syndrome, are those that improve insulin sensitivity, fatty acid metabolism and metabolic fitness.

It also is useful to consider here once again observations made in “Nutrient Combining”

• Low glycemic index diets improve glycemic (blood sugar) response and variability as well as promote the metabolism of fat for energy; they may promote longterm health.^21,22
• Taken in a milkshake, fructose (30 g) increased postprandial lipemia by 37 percent compared with control; glucose (17.5 g) increased postprandial lipemia by 59 percent.²³ (Lipemia is the presence in the blood of an abnormally high concentration of emulsified fat, meaning primarily triglycerides, not cholesterol.)
• In Syndrome X/insulin resistant subjects (BMI of 30), glucose consumption (50 g) led to a 15.9 percent greater glycemic response and a 30.9 percent greater insulin response than did fructose (50 g). This is true in part because fructose is processed in the liver and then released later as glucose and/or converted into fat.
• On an energy balanced diet in these same subjects, fructose compared with glucose increased carbohydrate oxidation 31 percent, but decreased fat oxidation by 39 percent.²⁴
• Low-fat/high-carbohydrate diets in Syndrome X individuals reduce levels of HDL cholesterol and increase triacylglycerol concentrations.²⁵
• Sucrose is glucose + fructose; lactose is glucose + galactose; grape sugar (dextrose) is glucose.

Conclusion
There is an old Chinese medical observation to the effect, “disease enters the body by way of the mouth.” Both the metabolic syndrome and non-alcoholic liver disease would appear to offer evidence for the correctness of this judgment. They also would appear to buttress another ancient opinion, this time from the ancient Greek physician Galen, who considered many of the conditions that today we associate as cardiovascular as arising from the liver and only subsequently manifesting in the heart, the circulation, and so forth. Liver health, as evidenced by subtle changes in certain markers, is closely linked to insulin sensitivity and energy metabolism. As such, the best approach to liver issues that are not related to the ingestion of toxins per se is to be found in diet and exercise habits.

Endnotes

1. Preuss HG, Mrvichin N, Clouatre D, Bagchi D, Preuss JM, Perricone NV, Swaroop A, Kaats GR. General Lack of Correlations between Age and Signs of the Metabolic Syndrome in Subjects with Non-diabetic Fasting Glucose Values. J Am Coll Nutr. 2017 Sep–Oct;36(7):556–64.
2. https://en.wikipedia.org/wiki/Transaminase
3. Porter SA, Pedley A, Massaro JM, Vasan RS, Hoffmann U, Fox CS. Aminotransferase levels are associated with cardiometabolic risk above and beyond visceral fat and insulin resistance: the Framingham Heart Study. Arterioscler Thromb Vasc Biol. 2013 Jan;33(1):139–46.
4. Magosso E, Ansari MA, Gopalan Y, Shuaib IL, Wong JW, Khan NA, Abu Bakar MR, Ng BH, Yuen KH. Tocotrienols for normalisation of hepatic echogenic response in nonalcoholic fatty liver: a randomised placebo-controlled clinical trial. Nutr J. 2013 Dec 27;12(1):166.
5. Loguercio C, Andreone P, Brisc C, Brisc MC, Bugianesi E, Chiaramonte M, Cursaro C, Danila M, de Sio I, Floreani A, Freni MA, Grieco A, Groppo M, Lazzari R, Lobello S, Lorefice E, Margotti M, Miele L, Milani S, Okolicsanyi L, Palasciano G, Portincasa P, Saltarelli P, Smedile A, Somalvico F, Spadaro A, Sporea I, Sorrentino P, Vecchione R, Tuccillo C, Del Vecchio Blanco C, Federico A. Silybin combined with phosphatidylcholine and vitamin E in patients with nonalcoholic fatty liver disease: a randomized controlled trial. Free Radic Biol Med. 2012 May 1;52(9):1658–65.
6. Aller R, Izaola O, Gómez S, Tafur C, González G, Berroa E, Mora N, González JM, de Luis DA. Effect of silymarin plus vitamin E in patients with non-alcoholic fatty liver disease. A randomized clinical pilot study. Eur Rev Med Pharmacol Sci. 2015 Aug;19(16):3118–24.
7. Sesti G, Fiorentino TV, Hribal ML, Sciacqua A, Perticone F. Association of hepatic insulin resistance indexes to nonalcoholic fatty liver disease and related biomarkers. Nutr Metab Cardiovasc Dis. 2013 Dec;23(12):1182–7.
8. Kawano Y, Cohen DE. Mechanisms of hepatic triglyceride accumulation in non-alcoholic fatty liver disease. J Gastroenterol. 2013 Apr;48(4):434–41.
9. Geisler CE, Renquist BJ. Hepatic lipid accumulation: cause and consequence of dysregulated glucoregulatory hormones. J Endocrinol. 2017 Jul;234(1):R1–R21.
10. Surapaneni KM, Vishnu Priya V, Mallika J. Effect of pioglitazone, quercetin, and hydroxy citric acid on vascular endothelial growth factor messenger RNA (VEGF mRNA) expression in experimentally induced nonalcoholic steatohepatitis (NASH). Turk J Med Sci. 2015;45(3):542–6.
11. Surapaneni KM, Jainu M. Pioglitazone, quercetin and hydroxy citric acid effect on hepatic biomarkers in Non Alcoholic Steatohepatitis. Pharmacognosy Res. 2014 Apr;6(2):153–62.
12. Scribner KB, Pawlak DB, Ludwig DS. Hepatic steatosis and increased adiposity in mice consuming rapidly vs. slowly absorbed carbohydrate. Obesity (Silver Spring). 2007 Sep;15(9):2190–9.
13. Ter Horst KW, Schene MR, Holman R, Romijn JA, Serlie MJ. Effect of fructose consumption on insulin sensitivity in nondiabetic subjects: a systematic review and meta-analysis of diet-intervention trials. Am J Clin Nutr. 2016 Dec;104(6):1562–76.
14. Softic S, Cohen DE, Kahn CR. Role of Dietary Fructose and Hepatic De Novo Lipogenesis in Fatty Liver Disease. Dig Dis Sci. 2016 May;61(5):1282–93.
15. Lim JS, Mietus-Snyder M, Valente A, Schwarz JM, Lustig RH. The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome. Nat Rev Gastroenterol Hepatol. 2010 May;7(5):251–64.
16. Lonardo A, Ballestri S, Marchesini G, Angulo P, Loria P. Nonalcoholic fatty liver disease: a precursor of the metabolic syndrome. Dig Liver Dis. 2015 Mar;47(3):181–90.
17. Bremer AA, Mietus-Snyder M, Lustig RH. Toward a unifying hypothesis of metabolic syndrome. Pediatrics. 2012 Mar;129(3):557–70.
18. Martínez Steele E, Baraldi LG, Louzada ML, Moubarac JC, Mozaffarian D, Monteiro CA. Ultra-processed foods and added sugars in the US diet: evidence from a nationally representative cross-sectional study. BMJ Open. 2016 Mar 9;6(3):e009892.
19. Monteiro CA, Moubarac JC, Levy RB, Canella DS, Louzada MLDC, Cannon G. Household availability of ultra-processed foods and obesity in nineteen European countries. Public Health Nutr. 2017 Jul 17:1–9.
20. Moreira PV, Baraldi LG, Moubarac JC, Monteiro CA, Newton A, Capewell S, O’Flaherty M. Comparing different policy scenarios to reduce the consumption of ultra-processed foods in UK: impact on cardiovascular disease mortality using a modelling approach. PLoS One. 2015 Feb 13;10(2):e0118353.
21. Henry CJ, Kaur B, Quek RYC, Camps SG. A Low Glycaemic Index Diet Incorporating Isomaltulose Is Associated with Lower Glycaemic Response and Variability, and Promotes Fat Oxidation in Asians. Nutrients. 2017 May 9;9(5).
22. Bennett CB, Chilibeck PD, Barss T, Vatanparast H, Vandenberg A, Zello GA. Metabolism and performance during extended high-intensity intermittent exercise after consumption of low- and high-glycaemic index pre-exercise meals. Br J Nutr. 2012 Aug;108 Suppl 1:S8–90.
23. Singleton MJ, Heiser C, Jamesen K, Mattes RD. Sweetener augmentation of serum triacylglycerol during a fat challenge test in humans. J Am Coll Nutr 1999 Apr;18(2):179–85.
24. Tittelbach TJ, Mattes RD, Gretebeck RJ. Post-exercise substrate utilization after a high glucose vs. high fructose meal during negative energy balance in the obese. Obes Res 2000 Oct;8(7):496–505.
25. Poppitt SD, Keogh GF, Prentice AM, Williams DE, Sonnemans HM, Valk EE, Robinson E, Wareham NJ. Long-term effects of ad libitum low-fat, high-carbohydrate diets on body weight and serum lipids in overweight subjects with metabolic syndrome. Am J Clin Nutr. 2002 Jan;75(1):11–20.

The post Liver Dysfunction and the Metabolic Syndrome appeared first on Total Health Magazine.

Commonly over the long term in type 2 diabetes mellitus, insulin resistances increases blood glucose levels followed by a compensatory rise in circulating insulin concentrations with the latter being the body’s attempt to adapt to the former. Consequences include high blood sugar levels, prolonged high insulin levels, the appearance of medical complications and the exhaustion of the pancreas’ ability to produce insulin.

The core of the metabolic syndrome thus is the dysregulation and dysfunction involving glucose and insulin. Aside from these, secondary characteristics encompass central obesity, hypertension, and dyslipidemias—especially hypertriglyceridemia and low levels of HDL cholesterol. In addition to participating in the development of many facets of the metabolic syndrome, impairment in insulin sensitivity also appears to be involved in the aging process by promoting inflammation, endothelial dysfunction, the production of advanced glycation end products (AGE), and oxidative stress. Downstream consequences of these dysfunctions include cardiovascular disease and cancer.

Several major questions have emerged regarding the appearance of the metabolic syndrome. Western medicine, unlike, for instance, traditional Chinese and Indian medicine, tends to pursue and treat the various arms of the metabolic syndrome as distinct clinical entities. Much of the research on the syndrome within allopathic medicine over the past three decades has been aimed at arguing against this separation. Another issue is the level of insulin resistance that should be taken as requiring attention. Most clinicians consider a level of circulating glucose under fasting conditions in the range of 100–125 mg/dl to be pre-diabetic. And then there is the issue of inevitability, which is to say, does the metabolic syndrome arise as a consequence of aging?

Early Signs of the Metabolic Syndrome in Non-Diabetics

For some time, there have been questions as to what should be acceptable as a normal fasting glucose level. Circulating glucose within levels generally accepted as normal can influence brain function in an unfavorable manner and increasing hemoglobin AlC (HbAlC) and insulin levels even in the non-diabetic range may affect blood pressure adversely. Such observations lead to suspicions that minor insulin resistance predicts the early onset of many disturbed health parameters involved in the metabolic syndrome. Recently Harry G. Preuss and co-authors, of whom I am one, addressed just such questions in “Fasting Circulating Glucose Levels in the Non-Diabetic Range Correlate Appropriately with Many Components of the Metabolic Syndrome.” ¹ Those with special interests should consult that journal and a forthcoming more detailed article.

To be sure, despite access to a large number of medical records, our study faced technical limitations. Because we worked exclusively with subjects possessing non-diabetic fasting glucose concentrations, the other measured clinical values, for the most part, fell in the accepted normal range. Therefore, correlations rather than exact numbers were largely used to determine alterations in health modalities. For corroboration, however, we examined statistical differences in the various parameters between the highest and lowest quartiles associated with these fasting glucose levels. Our data in this preliminary study are representative of the general population in middle and late middle age. The hypothesis is that glucose/insulin perturbations are at the heart of the increased incidence and severity of the various constituents making up the metabolic syndrome and could hasten/ worsen the aging process. A major goal in the study was to cast light on the issue of whether aging itself is associated with the development of the components of the metabolic syndrome or whether, to the contrary, containment of fasting insulin/glucose levels to a relatively low level reduced the appearance of the metabolic syndrome components despite advancing age.

Findings
Despite the fact that the population sample consisted entirely of individuals with fasting blood glucose readings below those of diabetes, there was a clear positive correlation between rising glucose levels and metabolic syndrome components. As expected, the average, baseline values of most parameters were in the accepted normal range. Nevertheless all of the following increased more or less in tandem with rising glucose levels: body weight, body fat mass, systolic/diastolic BP, HbA1C, circulating levels of insulin, triglycerides, hsCRP (highly sensitive C-reactive protein) and along with a number of other components representing inflammation and liver health. Elevated non-diabetic glucose levels were associated with signs of augmented inflammation (increased hsCRP, white cell and neutrophil cell counts) and liver perturbations (increased ALT) proposed to play a role in the metabolic syndrome.

On the reverse side, high-density lipoprotein (HDL) showed a negative correlation, meaning that higher blood glucose levels lead to lower HDL levels. Put another way, unlike fasting glucose, when total cholesterol became the independent variable, the majority of these health parameters improved showing beneficial correlations compared to fasting glucose. However, when examining the total cholesterol minus HDL-cholesterol correlations, all benefits of total cholesterol are lost, suggesting that the benefits noted with total cholesterol are primarily due to the presence of HDL-cholesterol.

We concluded that the early onset of the various risk factors correlating with circulating fasting glucose suggests a significant role for insulin resistance in the development of the metabolic syndrome. HbA1C and insulin values are also be linked to insulin resistance, but we chose to follow a more common, clinically available marker—circulating fasting glucose levels. Fasting glucose concentrations and the levels of HbA1C and insulin are significantly correlated, therefore findings are similar whether one tests using fasting glucose levels or insulin levels.

What is the ideal range of fasting blood glucose? Based on our preliminary study, the health data were significantly better with glucose levels in the range of 67–86 mg/dL than at 98–125 mg/dL. Across a wide range of variables, lower definitely was better. Another finding, one only touched on in the provisional version of the study described here, is that aside from blood pressure, age did not seem to play a significant independent role in determining metabolic syndrome health risks and even with regard to increasing systolic blood pressure (the top figure) the influence was less than expected. Glucose and insulin levels were the primary drivers of risk factors, not age.

Conclusion
If glucose and insulin levels are the primary sources of metabolic syndrome risks, then enhancing insulin sensitivity and lowering circulating glucose levels are steps that should be taken to promote and maintain health. Fortunately, many of the means to encourage better glucose control are relatively easy. Diet no doubt is key. Sugar, refined carbohydrates and excessive calorie consumption definitely are not friends of good health. Neither are bad eating habits, which include skipping breakfast, eating late in the day and snacking, especially at bedtime. Exercise can be very helpful, particularly taking at least a 15-minute brisk walk before lunch and again later in the day. All of these measures amount to the ounce of prevention advice that actually does work, but only so long as it is followed!

References:

1. Preuss, H. G., Clouatre, D, et al. Fasting Circulating Glucose Levels in the Non-Diabetic Range Correlate
2. Appropriately with Many Components of the Metabolic Syndrome. The Original Internist June 1, 2016, pp. 78ff.

The post Is the Metabolic Syndrome a Consequence of Aging? appeared first on Total Health Magazine.

In this article, I discuss the aging process in general for men, look at testosterone and hormonal changes, and then focus on maintaining prostate health and sexual function over the later years. And clearly for men, their prostate and sexual function are important to feeling youthful. Those that remain lovingly active, sexually and sensually, often feel better in many other ways as well.

Let me first say a few words about male aging, which I hope to experience, only very slowly with vitality and verve. We each have our genetics and biological clocks. Hopefully, if we play our cards right with healthy habits, understanding our risks and disease potentials, we can outlive our parents and ancestors. And for most issues of genetics and aging, lifestyle can trump our genetics and give us greater health and less disease.

Men need to look at and take action to prevent some of the common diseases that take us out of life too early. The big ones here are the cardiovascular diseases that start with inflammation, rising blood pressure, higher cholesterol, and subsequent atherosclerosis. The other is weight gain with rising blood sugar and insulin resistance of pre and early diabetes that speeds up cardiovascular problems. Lifestyle is so important to all of these common aging issues and helps in preventing, or at least delaying them. The lifestyle keys are focused on diet, exercise, and stress management.

Cancer risk is also a health and longevity threat, and here the colon and prostate are major concerns. These areas can and should be checked with some regularly to pick up any early changes. Colonoscopy, digital rectal exams, and PSA blood tests in men are well accepted for early diagnoses of these common cancers, although PSA tests have more recent controversy (as does mammography in women) because of potential fear and over-treatment that they can cause unnecessarily; also, there is controversy on how many of prostate cancers should be left alone and watched rather than suggesting and using aggressive treatments of surgery, chemotherapy, and radiation. Lung cancer is a minimal risk if you don’t or have not smoked. If so, regular chest x-rays are a test to consider.

It is important for men in the aging process to maintain normal weight, blood pressure, blood cholesterol, and blood sugar. Abdominal obesity from excess calories from refined foods, especially flour and sugars products, along with excess alcohol use can cause higher risks for many diseases. In current times, it’s easy to be overweight (or let’s say, harder to stay trim), however, research is showing that health and longevity can be protected with exercise and staying fit even with being somewhat overweight. A sedentary life with overeating and being overweight can create a high risk of disease and a shorter lifespan.

Tips for Healthy Aging

• Avoid Overeating and rich, fatty foods in your diet.
• Minimize Sugar, Flour, And The Many Refined Foods made from them as well as excessive alcohol.
• Maintain Normal Weight.
• Focus Your Diet around fresh vegetables with quality proteins and fresh fruit.
• Get Regular Exercise and avoid a sedentary lifestyle.
• Stretch to stay young and flexible.
• Stay Strong with weight training; muscle mass is important for healthy aging.
• Do Aerobic Exercise to stay fit and maintain endurance.
• Practice Stress Reduction such as meditation, breathing, qigong, tai chi, yoga, or relax out in nature.
• Listen To Your Body, and partner with your healthcare provider to address imbalances or symptoms such as sleep problems, digestive issues, sexual dysfunction, allergies, weight loss or weight gain, and stress issues; find ways that work to resolve these issues.
• Do Your Annual Physical Checkup to catch early signs of pending health problems.
• People Who Live A Long And Healthy Life tend to practice forgiveness, find a good balance between work and relaxation, feel gratitude and joy every day, nurture their creativity, stay connected with their friends and family, make a living doing something they enjoy, and use their talents and gifts to be of service to others. Wow! That’s another whole list.

HORMONAL CHANGES IN MEN

Many things change as we age, and this is true for blood levels of our hormones along with lower functions. For men, the many related hormones could become lower with time. This relates especially to testosterone, but also to thyroid and adrenal hormones, and less so to estrogen and progesterone. DHEA, or dehydoepiandrosterone, is a precursor substance that is produced form cholesterol molecules in the adrenals, and acts as a precursor for testosterone and estradiol. For both men and women, better levels of blood DHEA-S (sulfate) tends to be associated for both men and women with feeling better with a greater sense of well-being as they age.

In my office, I measure several blood levels when assessing men, especially over 40 years old. These include testosterone (often the total and “free” levels), DHEA-S, thyroid, and sometimes estradiol levels; if there’s fatigue I may order a 4-test saliva sample to check cortisol levels throughout the day. You and your doctor need to clarify the difference in test levels between the wide range of normal and more optimal levels.

If testosterone levels are low normal and there are symptoms accordingly, along with the person’s request to experience how they feel with some added body levels of circulating testosterone hormone, I will prescribe a topical hormone cream to apply daily for a couple months. Low male hormone levels can affect energy, mood, strength, sexual function, and vitality. After trying the treatment, we can evaluate the results and see what symptoms may have improved and how that correlates with blood or saliva levels of hormones. Testosterone can also be used as injection in oil, given every two-three weeks on a regular basis.

The use of testosterone replacement or enhancement in aging men is a controversial treatment. Over recent decades, it was thought to be cardio-protective as well as improve stamina and vitality; however, recent reports are suggesting that testosterone adversely affects the cardiovascular system. I don’t believe it as of yet, but it’s wise to review this aspect with your practitioner if you consider testosterone therapy.

PROSTATE PROBLEMS AND PREVENTIONS

It appears that the common disease among men over 50 (and now over 40) involves the prostate sex organ (and the colon, with stagnation and toxicity, diverticulitis and cancer). The Western lifestyle of stress and sitting plus often hours of driving and traffic, working, and TV watching; stuffing food and emotions; eating animal flesh and milk products; consuming sugary foods and caffeine; and using alcohol regularly—sets the stage for chronic, debilitating and degenerative diseases, such as cardiovascular problems, cancer, and arthritis, as well as prostate enlargement (BPH—Benign Prostatic Hypertrophy) and prostate cancer.

The prostate is a fibro-muscular organ, about the size of two walnuts placed together, and it sits at the bottom of the man’s pelvis behind the genitals and in front of the rectum. It can be felt (palpated) with the medical “digital exam” whereby a doctor sticks his gloved and lubricated index finger in through the anus and pushes forward. We should feel the pliable yet firm lobes without any enlargement, swelling, lumps or stony material. And the patient should not feel any pain, however, it could feel uncomfortable with a pressure like you have to urinate. Some symptoms of prostate enlargement or infection may be a pressure or swelling feeling in the perineum, or even more commonly, frequent urination and difficulty in starting or stopping urination. Men often need to get up two or three times at night to pee, which can lead to sleep issues as well. There may also be some change in the urine stream or force behind the urination. The ureter, or tube that passes from the kidneys and through the bladder, also goes through the prostate tissue and then through the penis. Thus, when the prostate is swollen, it may interfere with the urine flow.

A blood test can also be done to measure an antigen that is created by prostate cancer cells. It’s called the PSA (Prostate Specific Antigen) and if it’s elevated, that may mean prostate cancer is present. With inflammation or infection, the PSA can also go up; thus, it may need to be double-checked and/or rechecked after a course of antibiotics to treat any potential infection. If the elevation persists, even after any infection is treated, this may require further testing, as I believe it’s always wise to find out what is going on in our body. If it’s bad news, at least we can deal with it from there. Other tests to investigate the prostate further include a prostate ultrasound (sound wave assessment of the prostate tissue), a cat scan or the new body scan (both which utilize x-ray), and a prostate biopsy, which is usually done by an urologist. Luckily, many prostate cancers are slow growing or have not spread; yet they still can cause medical problems and metastasize over time.

The best overall plan, however, is to stay healthy and to maintain a healthy prostate.

As reviewed above, this involves staying young and in shape; maintaining sexual activity; getting regular exercise; managing your stress levels; taking stretch and activity breaks from long periods of sitting and computer work; eating a wholesome diet with lots of fresh veggies and quality proteins plus healthy fats; and avoiding excess substance use, especially of refined sugars, red meats and alcohol, while obtaining adequate essential fatty acids daily, such as two teaspoons of flaxseed oil, as well as adding fish oils and evening primrose oil. These are all ways that may help to prevent prostate problems.

Lycopene found in tomatoes (highest amount), watermelons, pink grapefruits, guava, and papaya is an antioxidant that mops up free radicals and helps protect the body against cancer. Cooked tomato products like tomato sauce allows lycopene to be more readily absorbed by the body. In research studies, two servings of tomato sauce a week are enough to lower the risk of developing prostate cancer.

Cruciferous vegetables such as broccoli, cauliflower, cabbage, Brussels sprouts, bok choy, collards, broccoli sprouts, Chinese broccoli, broccoli raab, kohlrabi, mustard greens, turnip, radish, rocket, watercress, and kale all contain sulforaphane, an anticancer and antimicrobial compound that helps the body repair damages caused by cancer cells while slowing down its growth. Another added benefit of eating these nutrient-rich cruciferous vegetables is the decreased risk for cardiovascular diseases while providing higher levels of vitamins and minerals that are also needed to prevent or fight cancer. The sprouts of these vegetable seeds, especially broccoli sprouts, have been shown to have anti-cancer effects.

Avoid charring meats when cooking (especially in grilling) to reduce the levels of a cancer-causing substance known as PhIP which has been associated to the development of prostate cancer in lab animals. Slow roasting, stewing, and broiling (without charring), are better ways to cook meats.

Zinc, selenium, Coenzyme Q10, vitamins C and E, vitamins K2 and D3, and the B vitamins, particularly B6, are all important for a healthy prostate, as are a number of herbs, which can also be used to treat prostate problems as well. There are two herbs that are specifically useful in preventing and treating prostate diseases, and thus, supporting sexual function. They are Serenoa repens and Pygeum africanum.

Saw palmetto berry (Serenoa repens) has been shown to effectively diminish pain, inflammation and enlargement of the prostate, as well as to reduce urinary urgency. It may work by inhibiting dihydro-testosterone (DHT), thereby reducing its stimulation for cell multiplication. Saw palmetto has been used for centuries and is also thought to have a mild aphrodisiac effect, as well as increasing sperm production and sexual vitality.

Another useful herb comes from an African evergreen tree, Pygeum (Pygeum africanum), and has been shown in research to reduce prostate enlargement and inflammation; it may also help stimulate libido. Pygeum has many natural chemicals that have anti-inflammatory and other positive effects on energy and bodily functions.

Some prostate formulas also may contain other herbs like nettle, or pumpkin seed extract or oil (higher in zinc and supportive of prostate health), and beta-sitosterol, a healthy fat that also supports prostate. Most men over 40-50 can benefit form the regular use of a good prostate health formula to both support this organ and prevent prostate problems.

The herbs and formulas work well and often at less expense and less potential harm or side effects than the popular drugs, such as Proscar or Flomax. These medications are typically prescribed by doctors for men with prostate enlargement or urinary symptoms.

Ultimately, it is conceivable that if we follow the aforementioned lifestyle advice, we can avoid treatment altogether and maintain both a healthy prostate and our sexual health and vigor. Long-term survival rate approaches 100 percent when prostate cancer is detected early. The ACS (American Cancer Society) recommends a PSA blood test and digital rectal examination be offered annually for men starting at age 50, although that is more recently questioned as to whether this test actually helps in saving or prolonging lives. Men in high risk groups, such as African American men, those with family histories of this disease, or with a history of rising PSA levels as well as altered levels of estrogen or testosterone, may begin testing at a younger age (i.e. 40-45 years). Men, who are not at high risk but are between 40 and 50 years old, may want to do both tests every two-three years.

It is far better to pick up any medical problems early, and this certainly applies to the prostate. Stay Healthy!

A good web site to keep abreast of prostate cancer research and treatments is www.ProstateCancerFoundation.org. Check out the latest research and guidelines.

The post Male Aging, Hormone Support, And Prostate Health appeared first on Total Health Magazine.

As a practitioner of energy psychology and follower of energy healing in general, I was intrigued. Then, after hearing him speak at the annual Energy Psychology conference in Toronto, (CAIET.org), I was hooked. Eric is funny, smart, and totally charming, more like a borscht belt stand-up comic than our usual notion of healer-speaker-expert.

Then I took the plunge and went to his annual Reconnection Healing seminar in Los Angeles. I was not disappointed; rather, I was educated entertained and uplifted. I saw with my own eyes how “spontaneous” healing can occur outside our usual belief systems of time and possibility. I was impressed at my ability and that of others to step into the process and have a real effect. They sure didn’t teach us this in medical school!

What Eric had accidentally stumbled across was what he describes as a “unique frequency or bandwidth” comprised of light, information and energy that actually corrects physical and emotional imbalances. As I learned in his seminar, he teaches people how to become a catalyst in healing others by learning how to interact with these new frequencies that “reconnect” us to our “original blueprint.” Stay with me here-there is some science to follow.

While seeing injured and chronically ill people get off a table instantly healed may seem like “magic” or “faith,” (and we know the power of the placebo effect) there is a growing body of hard science that is emerging on Reconnective Healing, explaining why it is a fast-growing new form of alternative healing world-over.

• Three major scientists are leading the inquiry—Dr. Kontstantin Korotkov, Deputy Director of Saint-Petersburg Federal Research Institute of Physical Culture;Dr. Gary Schwartz of the University of Arizona, and Professor Emeritus of Stanford University, and Dr. William Tiller (Stanford Prof. Emeritus) and founder of The William A. Tiller Foundation for New Science in Payson, Arizona. Dr. Tiller is the author of eight books, 250 scientific papers and star of the film What The Bleep…!? Four of his books are on psychoenergetic science.

Many of their studies are chronicled in the recent book, Science Confirms Reconnective Healing by Korotkov. Here are just a few of those findings:

• A former director of the University of Arizona’s Human Energy Systems Laboratory, Schwartz has performed multiple major controlled experiments there that have substantiated the electromagnetic transference in Reconnective Healing. Underway is a study measuring range of motion changes when the Reconnective frequencies are engaged.
• Tiller was able to gauge a huge energy upsurge in The Reconnection workshop rooms. Schwartz did a study that concluded aspiring Reconnective Healing Practitioners gain abilities to produce vibrational waves of energy via the Reconnective Healing that they learn at the seminars.
• Korotkov has demonstrated significant improvement in Olympic athletes’ peak performance once exposed to the Reconnective Healing frequencies. Energy parameters significantly increased almost immediately, while 10 days later their improvement became even more statistically significant. His studies have shown decreases in blood pressure, increases in metabolic, immune, antitoxin and antioxidant activity in the body, improved cardiovascular function and even improvements in their DNA.

What these scientists surmise from their findings is that Pearl is working with a cutting-edge new form of “information medicine”—in the words of Tiller—who explains further: “When information carried through these frequencies is introduced, it creates coherence and order within the field and the body itself.” The result can be seen in the dramatic reports of regeneration instead of degeneration, and account after account of apparently unexplainable, often instantaneous and life-long healings.

These bandwidths, which seem to be newly present in our planetary energy field, appear to innately “know” what needs to be healed. Pearl says that you are returned to an optimal and appropriate state of balance merely by experiencing or interacting with this healing continuum. The trained Reconnective Healing practitioner simply facilitates the process. By feeling the frequencies and playing with them—an act that appears as if the healer is stretching taffy in the air—physical and emotional health shifts suddenly come about.

We can see the impact on the person receiving Reconnective Healing as their closed eyes flutter and begin to rapidly dart back and forth, fingers or feet move as if of their own volition, and even involuntary muscles of the face move in a way that are unlikely to happen intentionally. All this occurs even though the practitioner isn’t even touching the client! These involuntary body movements—referred to as registers—are a demonstration that the client has entered into a different state, one where healing often occurs.

The information-laden frequencies reconnect us to our original fullness as human beings, according to Pearl, and seemingly restore us to a more complete connection with the universe.

More than a decade ago, when Pearl perceived the results of what was transpiring with his patients and saw its transformative power, he closed his practice as a chiropractor, so he could go out and share this skill with the world. Pearl’s book is now published in 36 languages and he has taught Reconnective Healing to 70,000 people around the globe in more than 70 countries.

Today when the cost of healthcare has skyrocketed and insurance is either unaffordable or barely covers what the average person requires to stay healthy, there is true benefit in literally taking healing into our own hands for ourselves, our loved ones and for those we can serve. Reconnective Healing, with its growing body of scientific proof and its legions of those who point to its efficacy, is a promising breakthrough.

While I am quite impressed here, both with my personal experience at the seminar, as well as the research data, I also know there are many other forms and schools of healing, some with their own well-documented research. Is this method substantially different from others? I invite your comments about how they compare, especially if you’ve had personal experience in any of these.

If you want to know more about about Reconnective Healing, go to: www.TheReconnection.com.

Citations from Science Confirms Reconnective Healing” by Konstantin Korotkov:

1. Korotkov K. Aura and Consciousness: New Stage of Scientific Understanding. St. Petersburg, Russia: State Editing and Publishing Unit—Kultura?. 1998
2. Korotkov K., Williams B., Wisneski L. Biophysical Energy Transfer Mechanisms in Living Systems: The Basis of Life Processes. J of Alternative and Complementary Medicine, 2004 10, 1, 49-57.
3. Polushin J, Levshankov A, Shirokov D, Korotkov K. Monitoring Energy Levels during treatment with GDV Technique. J of Science of Healing Outcome. 2:5. 5- 15, 2009?
4. Bundzen P. V., Korotkov K. G., Korotkova A. K., Mukhin V. A., and Priyatkin N. S. Psychophysiological Correlates of Athletic Success in Athletes Training for the Olympics; Human Physiology, Vol. 31, No. 3, 2005, pp. 316-323.
5. Measuring Energy Fields: State of the Art. GDV Bioelectrography series. Vol. I. Korotkov K. (Ed.). Backbone Publishing Co. Fair Lawn, USA, 2004. 270 p.
6. Korotkov K.G., Matravers P, Orlov D.V., Williams B.O. Application of Electrophoton Capture (EPC) Analysis Based on Gas Discharge Visualization (GDV) Technique in Medicine: A Systematic Review. The Journal of Alternative and Complementary Medicine. January 2010, 16(1): 13-25.
7. Korotkov K, Orlov D, Madappa K. New Approach for Remote Detection of Human Emotions. Subtle Energies & Energy Medicine o V 19, N 3, pp 1- 15, 2009

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