Tag Archives: arginine

THE CRUCIAL IMPORTANCE OF NON-ORAL ROUTE and LOWER DOSE OF SEX HORMONE REPLACEMENT SHRT in the majority-the overweight, diabetic, cardiac, thrombosis, transplant, dementia and cancer risks.

Obviously our   skin (unless injured or diseased) – arguably our  major organ of heat control, sweating, vitamin D activation  and sexual enticement- serves as a major impenetrable barrier to  absorption or leakage. Unlike amoebae- which live or die by their exterior- we feed and excrete via our digestive tract, using our skin mainly for attraction-  or repulsion!.

It is common cause that, with intravenous injection ivi as the fastest alternative route (to swallowing), absorption is hardly better (than the skin) across aged dry vagina; better across moist ie mucous membranes eg of the eyes, nose, mouth and vagina/rectum; better by deep inhalation or subcutaneous s.c. placement (injection or pellet); and best  by intramuscular injection imi – which is now rarely achieved with  a standard 3/4 inch needle into the upper outer buttock in a fattening population . Such injections are mostly delivered s.c.

Which route is preferable depends obviously on the speed of action required eg high blood peak for an urgently needed antibiotic, analgesic, anaesthetic, antiasthma, acute insulin or resuscitation; as opposed to slow smooth delivery for maintenance eg hormone, antidepressant or analgesic delivery.

For depot injections, why use anything bigger than a 25g 10mm long needle?  so that safe subcutaneous   s.c.i.  is ensured,  guaranteeing  avoidance of the many minor and major risks of intramuscular   imi.

eg Meyer ea at Cornell Univ NY 1990 reported  that subcutaneous administration of the gonadotropin releasing hormone agonist leuprolide took half the time to first response with double the amount absorbed compared to the same dose by the transdermal TD route.

Minto, Handelsman ea in 1997 showed that injection of an oil-based depot sex hormone into the fattier gluteal (ie upper outer buttock) region (as compared to the lean deltoid ie upper arm true imi) gave significantly slower smoother less peaked absorption and action of the hormone.

And obviously total delivery to the body is going to be less absorbed  through the tightly layered  skin than if 100% delivered under the skin by injection/implant. Fatty – steroidal- gonadal hormones are particularly altered by digestion and transhepatic absorption. But so will transdermal absorption fall with aging, drying of the skin.

Hence in postmenopausal women PMW  the average dose equivalence for similar symptom- hot flash- relief has been found to be estradiol 1mg or CEE 0.625mg orally, but about 0.05mg E2  a day by modern TD designer patch (containing 4mg E2, changed twice a week)  or cream;  ie an effective oral: TD dose ratio of about 20:1. But  oral estrogen eg 1mg E2 raises the E1 estrone (the hormone most associated with breast cancer) blood level  5-fold more than the E2 level, and increases urine estrogen excretion about 100fold; whereas the E2 patch 0.05mg/day raises serum E2 to a satisfactory ~120pmol/L  but with  little  increase in E1 level  or urine estrogen excretion. Thus TD but not oral ET restores the youthful healthy balance of blood E2>E1 aout 1.2 :1.

Conversely, in  girls with delayed puberty and growth,   physiological effect appears to be even higher with TD estradiol  E2  than oral conjugated oral estrogen CEE Premarin. In a recent trial undeveloped girls with Turner’s syndrome were randomly assigned to receive initially  CEE 0.3mg/d orally, or TD E2 0.025mg/d patch (17β-estradiol, Vivelle TD) for one year – doses chosen based on published E2  equivalence  about 20:1. After 12 months the girls on TD ERT had better improvement in uterine, height, breast, and bone density growth than oral HT CEE. Hence they too (like postmenopausal  PMW) needed far lower total dose estrogen exposure parenterally than orally. PMW certainly rarely if ever want bigger breasts or womb, so even lower transdermal microdoses are ideal for them.

Nachtigal ea 2009 show that oral but not TDE2 accelerate platelet reactivity ie thrombosis risk in some PMW.

Villa ea 2008 show that low dose 1mg/d micronized E2  lowers insulin resistance, whereas higher dose 2mg/d increases it.

Verhoeven ea 2006 showed that oral micronized E2, but not TD  E2 treatment, significantly reduced arginine compared with placebo – and good arginine levels are crucial in maintenance of immunity; insulin sensitivity;   growth hormone output; wound repair; fertility; and adequate nitric oxide levels for optimal muscle, heart and circulation..

And Shifren ea 2008 showed that compared with oral CEE, TD E2 exerts minimal effects on CRP and the other inflammation and hepatic parameters – more adverse hepatic first-pass effects of oral HT as regards both cancer and cardiovascular disease. .

Thus, given that the higher the rate of breast and uterus proliferation the greater the risks in later life, sex hormone therapy and replacement in women (let alone men) should always be parenteral- the lowest dose to achieve the desired goal- be it feminization in Turner’s Syndrome; contraception; or postgonadopausal HRT in men or women.

The ill-informed reaction to the poorly planned Womens’  Health Initiative led to a massive fall in all HRT use.


Yet abundant studies reviewed in this column the past two years show the incalculable benefits of appropriate balanced (E+P+T) in PMW.  No-where is this better shown than in neuroprotection especially against Alzheimer’s disease AD, in which- in eg  the Womens’ Health Initiative–  introduction  of oral xenohormones well after age 60years worsened the risk of AD, but  CEE  started soon after menopause greatly reduced AD risk.

University   Beijing has shown that women who have taken lowdose oral E2 0.5-1mg plus progesterone 0.5-2mg for 4 to 33yrs have  significantly less hippocampal atrophy;   similarly at Univ S California,  studies in AD-prone mice show that early oophorectomy worsens the AD pathology and behaviour changes, but this deterioration is better blocked by E2 + progesterone combined than by E2 alone.

Testosterone replacement is probably brain-protective in men;  it remains to be seen whether it adds  memory protection in women when combined with E+P. A  2006 British study of estrogen treatment in male to female transsexuals showed few and inconsistent changes in memory and cognition.

But a new Spanish study does show that when female-to-male transsexuals are treated with testosterone for 6 months, they show significant improvement in visual but not verbal memory.  And a new Swedish study shows that “The most positive effects of estrogen plus progestogen therapy concerning memory and urinary tract and vaginal complaints were found in women with the highest and/or moderate testosterone levels (P < 0.05).”

recent UK  MRC study shows the critical importance of optimal thyroid function in memory, since excess of either thyrotropin or thyroid hormone can be adverse.

And it has long been known that the more hypoglycemic episodes diabetics experience, the worse long-term memory.

Thus balance of  all three major sex hormones- estrogen, testosterone and progesterone, as well as insulin and the thyroid axis,  is  crucial in cognitive performance especially in women.

HORMONE CREAMS: for those who prefer creams to  pills, implants or injections, a major advantage is that  women  can start low with all three main sex hormones as appropriate, and titrate them individually upwards to tolerance or designated ceilings. Once optimal intake and levels of each have been attained, they can then if wished be combined, compounded.


As this column discussed two weeks ago: mid- twentieth-century women now potentially live to double the age of those born in the early Victorian era; but increasing numbers undergo premature menopause and especially relative androgen deficiency due to  elective sterilization, hysterectomy, survival from cancer and radiotherapy, or increasing cancer risk from smoking, alcohol, suppressed menstruation due to birth control hormones, cortisone use eg for autoimmune diseases and transplantation, nuclear fallout or the feminization of nature .

They thus spend the second half of their lives post menopause, with increasing premature mortality and morbidity from diseases of hormone deficiency:   fattening and diabetes; heart and circulatory disease; muscle and bone frailty; arthritis; infections,  incontinence;  and worst of all, depression,  cancer  or loss of memory; and not least, loss of vital  sexuality. These are all largely avoidable by appropriate early and permanent non-oral balanced HRT and a blend of the other three-score other natural  supplements.

As Prof  Robert Greenblatt from Augusta  wrote in The Menopause Syndrome (Medcom Press)  in 1974, ” the menopause is a physiological endocrine hormone deficiency state. It is good practice to offset endocrine deficiency states by hormone replacement therapy to restore hormone balance”- whether in a teenager or a grandmother.

And Prof Emanuel  Schleyer-Saunders from London stressed in the same colloquium that even 35 years ago, half of all hospital beds were occupied by diseases of old age- obesity-diabetic-vascular, mental and malignant- which (as Masters and Grody had shown 20years earlier) are delayable by decades provided balanced parenteral permanent HRT is started early in menopause- which starts insidiously in the mid-forties if not earlier.

Whereas Masters and Grody in St Louis, and Gelfand in Quebec,  established this by long term injections of testosterone TT and estradiol E2  esters (which for decades have been available as a 20:1 mixture lasting 2 to 3 weeks), Schleyer-Saunders and then Whitehead and Studd  in London,  and Gambrell in Augusta, maintained this long term by pellet implants every few months.  Schleyer-Saunders showed with pellets that continuous balancing TT reduced the incidence of breakthrough bleeding from 20% on E2   alone , and 12% on E2 + progesterone P, to 8% on E2 + TT,  but only 5% on all three ie E2 + P + TT – with reduction in cancers. He generally used a dose of 25mg of each hormone, but (at a time when  women were far slimmer) 50mg E2 implant  in women post oophorectomy.

Yet MacLennan ea from the International Menopause Society now report that in Australia, as a result of the hysteria generated by the wrong Womens’ Health Initiative and Million Women Study reports (in which most women used oral xenoHT), only 12% of postmenopausal use hormone replacement.

Convenience should be the last factor considered. Unless balanced  lowdose mcronized estradiol, testosterone and progesterone are used orally  – since micronized particles largely  bypass  transhepatic absorption- there is no longer excuse for the risks of oral CEE,  progestins and similar hormone therapy with hepatic first pass adverse effects.  “Convenience” is no defense  against charge of negligence  when the patient develops major complications from oral sex hormones. So the patient who insists on oral hormones should sign an informed consent form that she has been warned,  but accepts the risks of the oral (as opposed to the physiological parenteral) regime.

All  women (and men) – especially with chronic or serious acute ill health – should thus be ensured  permanent  youthful sex hormone levels with appropriate physiological HRT that avoids both hepatic first pass metabolism and hormone excess/ imbalance. Traditional American industrial hormone therapy ( dominant the past 50 years due to the connivance of the FDA with it’s supporting drug industry) with oral xenohormones eg CEE, progestins and anabolic steroids cannot provide the physiological replacement required, that is ensured with titrated human hormones  in every other branch of endocrinology for the past generation.

It remains an indictment of American medicine and legislators that their Disease and Drug  Industry- the FDA and mainstream physicians-   put their  commercial interests ahead of  womens’ welfare   in making postmenopausal women the exception to the rule of  evidence-based medicine especially endocrinology. The most vulnerable group (after children)- the older women – are thus as always the main innocent victims of the FDA-led  Disease Industry’s  War on Humanity, the Black Mass of organized commercial Big-Pharma “medicine”- of which 13  USA firms in  about 2006 had half the world’s gross “medicines” turnover of ~ $600billion. Based especially  on womens’ ills and vulnerability- particularly cosmetics and cosmetic surgery, screening mammography and hysterectomy-  the Beauty/Disease Industry is thus truly a multi-$trilliondollar moneyspinner, disaster capitalism targeting women.










ABOUT FATS & CHOLESTEROL: Most nutrients – sugars, proteins and micronutrients-  are water-soluble:
Water abounds -we are ~30% to 75% water depending on how fat we are;
and water-soluble vitamins, minerals,  sugars, proteins and other nutrients abound  in our food chain.
It is common cause that the water-soluble vitamins – (the nine  vitamins B plus vitamin  C)- give enormous  extra multisystem protection in safe megadose supplement. These are ubiquitous if often inadequate for modern pollution, stress and epidemics  in the average  urban (or rural poor) raw and even in the lightly cooked produce/  food-chain we eat.

FATs include both the solid and the liquid form; but “fat”  – ie (semi)solid at body  temperature- is ubiquitous in human diet; once cooked, animal or vegetable or dairy , its all the same saturated sludge. Except in milk, fat is solid in animals and produce, as anyone who has had a deep cut knows- it doesn’t run out!

Expressed uncooked plant oils ie liquid at room temperature, or as the natural vegetables,  are much better  for health than cooked or animal fats,    But  they are largely omega 6 / 9 (like the omega 6 arachidonic acid in meat); and if indeed plant oils provide  omega 3, it is    ALA- alpha-linolenic acid  , not the crucial essential marine omega 3  eicosapentanoic EPA/ docahexanoic acid DHA – to which ALA is poorly converted by humans..
As opposed to oil,  FATS in humans appear to serve only a few purposes: energy storage for times of starvation; insulation against cold and falls; and synthesis of eg estrone and leptin. But the higher the fat stores, the greater the risk – eg vascular sludging (ie grime), cancer, inflammation, and trauma to weightbearing joints eg the spine, hips, knees etc.
In temperate climates, human adults carry  ideally at most 13 – 15% fat (except for women wanting to fall pregnant, when about 20-25% fat is optimal – Beth Frisch’s  hypothesis).
OIL on the other hand  is essential for lubrication in both engines and animals- and with the oil-soluble micronutrients  especially the EPA-DHA and the sex hormones – for  supple skin, mucosa (eyes, mouth, vagina), joints muscles ligaments and tendons, brain and heart . But many choose to ignore this crucial deficiency  in aging people, and instead prescribe toxic designer  “anti-inflammatory” drugs, or omega 6.
List of essential nutrients :- Wikipedia gives a useful list of the traditional dozens of essential nutrients : but this list includes many which are adequate in a prudent diet.
But the growing “news”  is on the rediscovery of the crucial protective role of appropriate  fat-soluble supplements for prevalent diseases – stress, pollution and aging eg the marine omega3 EPA and DHA;  fish oil; coQ10,  vitamin K,  and the steroids vitamin D, testosterone, progesterone and estrogens;    as opposed to the water-soluble crucial micronutrients eg arginine, carnitine, coQ10, ribose, N acetyl cysteine; glucosamine-chondroitin; lutein-zeaxanthine, essential minerals etc.
FAT SOLUBLE MICRONUTRIENTS however, are far fewer than water-soluble micronutrients, and thus have even more important diversity and potential deficiencies since our primary physical anatomy is the fatty cell membranes, and our fatty mammalian nervous systems (about 8% fat, 80% water, 10% protein):
CHOLESTEROL is obviously the crucial basic building block for cell membranes, and steroids – which we lower too far (with eg starvation or  statins) at our grave peril.  Cholesterol–  the principal sterol synthesized by animals-  is an essential component of mammalian cell membranes to establish proper membrane permeability and fluidity.  Minimum levels of cholesterol are essential for life.  Cholesterol may act as an antioxidant, in the manufacture of bile and helps digest fat, important for the metabolism of the fat soluble vitamins A, D, E and K., and is the major precursor of the various steroid hormones (which include cortisol and aldosterone, and the sex hormones progesterone,  estrogens, testosterone). It also covers nerves in the form of myelin, to conduct nerve impulses.    Recently, cholesterol has also been implicated in cell signaling processes. But since the liver makes about 1gm cholesterol a day, it is not essential in the diet.

1. FISH OIL– perhaps the most important supplement there is-  as the till-now unique and only source of the essential fatty acids EPA and DHA, is discussed at length.
Along with nuclear fallout), we  WW2 & baby boomer generations got plenty of fish oil as kids  – in breast milk; as cod liver oil in malt; or  provided fish was lightly cooked, or raw- sushi or eg pickled (not cooked) herring (not fried). And of course there were plenty of oily fish around- sardines, anchovies, pilchards, mackerel, tuna, salmon, cod. But these are now increasingly scarce, or polluted whether wild or farmed. We now rarely find even canned pilchards or salmon with the fish oil left in the cans- it is usually run off and replaced by harmful saline or plant oil. And northern hemisphere fish is increasingly contaminated by heavy metals let alone synthetic xenoestrogenics  like dioxin, PCBs, insecticides etc which are rapidly sterilizing the planet (look at the 90% fall in the bee population in N America- no bees, no cross-pollination, no flowers, no plant produce). .
So we now all need to take fish oil to get our essential minimum 800mg EPA+DHA a day.
A popular myth is heavy metal contamination of fish oil. But  toxic heavy metals are water-soluble and bind heavily to proteins, so there are none in clean commercial fish oils. see 1, 2 – which are indeed  rigorously controlled for deadly industrial  solutes like PCBs, DDT, dioxin.

In Alzheimer’s disease, the latest research affirms the likely protective role  especially for  the elderly of early and permanent fish oil supplement ie DHA; and the harm of supplementing plant oil ie excessive arachidonic acid.


2.1 VITAMINS A- CAROTENOIDS– the provitamin A beta-carotene β,β-carotene  – is crucial in supporting skin, vision,  memory, and immunity against infections eg viral. Patients with acne have been shown to have low blood levels of vtamin E and especially vitamin A. Beta-carotene is composed of two retinyl groups, and is broken down in the mucosa of the small intestine  to retinal, a form of vitamin A.. so supplementing b-carotene provides us with vitamin A as we require it.
There is apparently no toxic dose of bcarotene C40H56, but prudence- if only to avoid yellow skin- is not to much exceed 15000iu/day;   whereas excessive vitamin A –retinol  C20H30O-  dose increases incidence of some cancers eg in smokers.
No trial has been published comparing head-on the patented (vitamin A- modified)  oral designer drug isotretinoin Roaccutane C20H28O2  with combination of the skin nutrients: beta carotene C40H56  plus vitamins B C D E plus fish oil and zinc. Since most of the latter have proven major anticancer, antiviral, cardiovascular and antidiabetic as well as (like betacarotene) antiinfective, skin and memory benefits, there is no comparative evidence to justify except as last resort  the use of toxic isotretinoin for cystic acne, especially not in children.

The careteinoids C40H56O2 lutein and it’s isomer  zeaxanthine are crucial in protection against visual loss- macular degeneration- and Alzheimer’s disease.

2.2 VITAMIN D There is a flood of new research  papers recently  on the importance of vigorous (not traditional 400iu/d) vitamin D supplement   against  all major acute and chronic diseases including infections.
It becomes clear that we optimally need vit D  bloodlevels of ~80-120nmol/L, ie  5000iu to 10 000 iu/d rather than 400-800 iu/d,  just as men and women  need testosterone .
There are now well over fifty conditions associated with suboptimal vitamin D levels. (adapted from Dr Joe Mercola) :

dermatoses: eczema; acne,  Psoriasis ,lupus. Multiple Sclerosis
Alzheimer’s disease Diabetes 1 and 2 Muscle pain

IgA nephritis

Asthma Hearing loss Obesity
athleticism impaired Heart disease osteoporosis
Autism Hypertension Parkinson’s
cancer* hyperactivty learning disorder, ADHD Periodontal disease, cavities
chronic fatigue infertility  miscarriage prematurity pre-eclampsia prostatism, BOO
infections; Septicemia Insomnia Rheumatoid- & osteo-arthritis,SLE
Crohn’s disease learning disorder schizophrenia
Cystic fibrosis; COPD Macular degeneration; myopia seizures
Depression Migraines thrombosis

*cancers of  breast, colon ovary kidney and endometrium occur much less in sunny places in the world.

One cannot  find a major acute, or  chronic, youthful  or degenerative  aging, disease not on this list;     and only fish oil may have wider benefits.   Even age-related lung function decline has strong inverse relationship with baseline vitamin D level; which is not surprising considering how osteoporotic shortening and bowing restricts the lungs, and lack of vtamin D weakens muscles.
So perhaps only  regular outdoor workers – hikers/bikers/swimmers –  with strong muscles and bones need not worry about their vitamin D level.

But the cost of a vitamin D3 measurement is awesome  in RSA (R660) or about US$66. Ultrasound BMD sceening is a  more affordable indirect screen, with checking of calcium bloodlevel occasionally so as not to overdose vitamin D.

Vit D production  from sunshine apparently self-limits vitamin D production for safety to about 400 to 2000iu internal synthesis/day. Vit D in cod liver oil is regulated by treaty to  about 100iu/gm oil.
The manufacturing industry has reportedly, without announcing it, redefined and sells “pure” vitamin D powder as 100iu/mg instead of the scientific standard  40 000iu/mg; thus what they sell  as pure  “vitamin D3” is actually 0.25% . So we have to pay freight for 99.75% inert filler to be shipped around the world. This too is the standard commercial fraud.

So for  the benefits of safe vigorous vitamin D 6000iu/day or 50 000iu /week, we need a vit D supplement.

2.3 VITAMIN E the mixed tocopherols are most important fat-soluble antioxidant   vasodilators; but dose should not exceed about 1600mg 800iu/day since, like betacarotene, this vitamin in excess is  associated with increased lung cancer when combined with the 4000 carcinogens that smokers choose to ingest . Supplement of vitamin E may benefit circulation, Parkinsons, Alzheimer’s or visual loss.

2.4 VITAMIN K supplement has recently  appeared to  be almost as important as vitamins  D and C supplements in preventing not just warfarin dose instability,  but also osteoporosis fractures, cancer and cardio/ vascular disease. The only major difference is that vitamin K supplements do not appear to reduce infection- but vit K supplement may be safe & worthwhile during/ after antibiotics to avoid vitamin-K deficiency (and thus bleeding and increased vascular, bone and cancer risk ). In the recent ECKO trial from Univ Toronto (Cheung 2008) , vit K just 1mg/d halved fractures in postmenopausal women over 2 -4yrs despite no clear increase in bone density.


3.1 THYROXINE T4 AND TERTROXIN T3 are  the  crucial fat-soluble thyroid hormones (combined in Diotroxin) which especially after mid life often require replacement for either poor thyroid production or for resistance due to antibodies.


3.2.1 CARDIAC GLYCOSIDES eg digoxin are hydrophilic ie fat-soluble natural steroids from plants and animals (apparently from our adrenals and brain)  that strengthen heart contraction and slow the heart in preventing/ treating rapid atrial fibrillation. Obviously we have evolved them too over a million years, and plant glycocides have been used medicinally for centuries if not millenia.

3.2.2 ADRENAL: CORTISONE (and ALDOSTERONE)  are also  crucial fat-soluble adrenal  steroid  hormones which may with aging or stress burnout (type C personality) justify  replacement orally for relative if not absolute cortisol deficiency.

3.2.3 SEX HORMONES: the  all-systems ie anti-aging benefits of lifelong parenteral primary  human sex hormones  testosterone, estrogens, progesterone  (from the gonads and adrenals)  have  been documented for millennia, and confirmed for sixty years with their appropriate supplementation- reducing all-cause mortality and morbidity by at least 1/3- especially testosterone and it’s daughter estrogens for men and women; and increasingly in new studies that parenteral estrogen halves the risk of heart attack post menopause.    eg .https://healthspanlife.wordpress.com/2008/11/05/proof-again-parenteral-estrogen-halves-the-risk-of-heart-attack-post-menopause/.

The American National Osteoporosis NOF website for patients  has legion bewildered queries from  patients being told dogmatically by their  doctors that they must take new  (risky and long-term unproven) designer patent  single-target  ie fraudulent drugs eg bisphosphonates, strontium ranelate  for osteoporosis – not the old and proven  safe dozen appropriate  natural multisystem supplements that combat all chronic major degenerative diseases as well as optimizing childhood development, learning-memory, and defence against  infections –  ie the freely available  vits B 6,9,12, C, K, calmag, zinc, boron, manganese, proline, fish oil, and for sexhormone imbalance/ inadequate levels, appropriate testosterone for both sexes plus appropriate parenteral estrogen for women (or occasionally DHEA where appropriate). .

4. CoQ10 ubiquinols :    these vital antioxidant insulin sensitizers appear beneficial in doses of up to 300mg/d against heart failure ; cancer; migraine; Parkinson’s; oral-gingival disease; Alzheimer’s; hypertension; COPD; and cardiac arrest.
Compared to niacin, fish oil, CoQ10 and other insulin sensitizers, there is no justification for the use of statins for mild-to-moderate  lipidemia, when these synthetic designer drugs are a cause of coQ10 depletion (reported repeatedly since 1990)    and  do nothing for non-cardiovascular disease and mortality including insulin resistance;
and when (because drug companies will not risk head-to-head trials of statins against alternatives)  there is no evidence  that statins are as good  (against mild-moderate  hypercholesterolemia-associated CVD) as eg niacin and other vitamins-minerals, fish oil, metformin, coQ10, arginine, carnitine, ribose,  and other insulin-sensitizing antioxidants;
and when supplementing CoQ10 also does nothing for the myopathy let alone impotence caused by statins.

FAT-SOLUBLE POISONS STORED IN BODY FAT such as DDT or PCBs, are also stored in the fatty tissues, but the body has no use for these substances and they are NEVER withdrawn from these fatty tissues for any valid use within the body.
These harmful chemicals (DDT, PCBs) do leak out of fatty tissues (during times of sweating, for instance), but when that happens there is no beneficial use for them in the body — and they cause far more harm  than good after they have leaked out.
Worse, these poison are stored in the body fat of all flesh we eat (just as heavy metals are stored in protein ie muscle); hence vegetarians run lower risk.
Worse, aluminium (which is not usually water-soluble) accumulates in  the brain (let alone bone), and is one of the few minerals that has no known biological benefit, but contributes greatly to dementia and fractures.
Worse, there has been massive pollution of reserves by recycled water effluent from sewage works and industry, leading to global fauna sterilization /destruction by the masses of contraceptive and anabolic steroid hormones prescribed for humans and  animals (Deborah Cadbury: The Feminization of Nature 1997 )  that threatens to sterilize and thus wipe out most of humankind this century.
And worst of all, deliberate adulteration of commercially grown meat/fish for accelerated growth by anabolics – especially the high-risk synthetics like ethinylestradiol and progestins- is especially poorly regulated since the industrialized countries  notoriously dump these (as well as stocks of eg dangerous insecticides, and genetically modified seeds)  via ruthless politicians/middlemen on poor countries like South Africa  where there is minimal monitoring of transgressions.

NON-ESSENTIAL “ESSENTIAL” (PLANT) OILS eg from cloves, tea tree, garlic,  mrenthol, eucalyptus, citrus, rose, may indeed have medicinal benefits used topically/ in aromatherapy; but are outside the scope of this review since they are not human biologicals like the vitamins, steroids and essential fatty acids..
IN CONCLUSION: whether by design or random evolution, we developed dependent on if not from  sea life, and especially marine oil, fat-soluble micronutrients; but with longevity, and as we become eaters of largely cooked flesh and produce, with depleting marine fish reserves, we need marine oil and fat-soluble micronutrients ever more- not processed plant oils and cornstarch.
It’s like all other natural supplements and valued old products:
Nothing has yet contradicted  that metfomin (a plant extract) is the last “synthetic” ie drug industry  designer preventative  for chronic prescription use that actually reduces all-cause mortality and morbidity ie is the panacea; without enough insulin sensitizers, excess calorie are simply diverted to more cholesterol and body fat;

while  the natural supplements: FAT-SOLUBLE  fish oil; vit D3; and testosterone, +-  extra estrogen  for women  – look like they may prove equal  to if not better than metformin solo as panaceas.

You can’t beat nature/creation  for providing healthy options;                                                                      nor  endless human greed in trying to do better for profit by promoting designer substitutes?

If we continue to destroy species -especially marine life- at the rate mankind is doing, there will soon be no marine life- EPA/DHA – left- and  the science industry  (unlike nature) has yet to work out how to make them.

How to Survive a Heart Attack When Alone: coughing and deep breathing? too little too late.

How to Survive a Heart Attack When Alone: coughing and deep breathing?
This email doing the rounds may be inappropriate advice that could cost people their lives. – see http://www.hoax-slayer.com/survive-heart-attack.html and http://www.viahealth.org/body_rochester.cfm?id=329

BUT an apparently reputable cardiologist (apparently ex Vietnam Medic) also recommends it: http://www.karinya.com/cpr.htm

BUT see the notes of caution at http://en.wikipedia.org/wiki/Cough_CPR.

In short, it may save those who have sudden arrhythmia- but it is less likely to save those who are having a huge heart attack.- for whom most interventions are too late. The compromise may be to switch on the vehicle’s emergency flicker, stop the car, start coughing while collapsing visible over the steering wheel with a hand on the hooter to attract attention..

Very very few people recover or survive well long term after spontaneous (ie non-violent, non-toxic) cardiac arrest outside hospital – the studies below from France, Germany , USA & UK indicate that successful survival without impairment is – in the best hands – below perhaps 5%. .

So only primary prevention pays. Fish oil halves sudden death; metformin halves the deathrate in type 2 diabetics – and halves new diabetes in the overweight; appropriate estrogen replacement lowers allcause premature mortality by a third; deficiency of testosterone, estradiol, minerals, vitamins, CoQ10 , arginine, carnitine and ribose play a crucial role in the development and reversibility of arrhythmia, cardio/vascular and all-cause degenerative disease; and testosterone is antiarrhythmic but estrogen arrhythmogenic.

By contrast, unlike the above proven life-extenders, no modern designer drugs for chronic use have been shown to significantly reduce all major chronic degenerative diseases and premature all-cause mortality.

Thus all should take natural supplements early and permanently – appropriate vigorous supplements of minerals, vitamins and biologicals (including fish oil, insulin sensitizers and sex hormone replacement), to minimize early vascular disease and arrhythmia potential.


Heart. 2007 ;93:601-5. Sudden arrhythmic death syndrome SADS : a national survey of sudden unexplained cardiac death.Behr ER, Casey A, Sheppard M, University of London, UK. The estimated mortality from SADS was 0.16/100 000 per annum (95% CI 0.12 to 0.21), compared with an official mortality of 0.10/100 000 per annum for International Classification of Diseases 798.1 (sudden death, cause unknown-instantaneous death) or 1.34/100 000 per annum for unascertained causes of death. CONCLUSIONS: Deaths from SADS occur predominantly in young males. When compared with official mortality, the incidence of SADS may be up to eight times higher than estimated: more than 500 potential SADS cases per annum in England. Families with SADS carry genetic cardiac disease, placing them at risk of further sudden deaths. SADS should therefore be a certifiable cause of death prompting specialised cardiological evaluation of families.

European Heart Journal 2006 27:406-412 Post-discharge survival following pre-hospital cardiopulmonary arrest due to cardiac aetiology: temporal trends and impact of changes in clinical management Jill P. Pell ea University of Glasgow,
The Heartstart Register was used to identify all 1659 patients discharged alive from Scottish hospitals during 1991–01 following pre-hospital arrest due to cardiac aetiology. Over the period studied, the proportion of people suffering pre-hospital arrest who survived to discharge from hospital changed from 11.6% (552/4766) in 1991–93, to 7.0% (558/8006) in 1997–01.

Resuscitation. 2005 65:49-55. Outcome after cardiac arrest: predictive values and limitations of the neuroproteins neuron-specific enolase and protein S-100 and the Glasgow Coma Scale. Pfeifer R, ea University of Jena, Germany.
BACKGROUND AND PURPOSE: Patients resuscitated from cardiac arrest are at risk of subsequent death or poor neurological outcome up to a persistent vegetative state. We investigated the prognostic value of several epidemiological and clinical markers in 97 patients undergoing cardiopulmonary resuscitation (CPR) after non-traumatic cardiac arrest between 1998 and 2002. RESULTS: 72.% of the patients died or remained in a persistent vegetative state; and 28.8% survived with severe, moderate or without neurological disorders. .

N Engl J Med. 1999 341(8):569-75. A comparison of standard cardiopulmonary resuscitation and active compression-decompression resuscitation for out-of-hospital cardiac arrest. French Active Compression-Decompression Cardiopulmonary Resuscitation Study Group.Plaisance P, ea .Lariboisière University Hospital, Paris, France. BACKGROUND: We previously observed that short-term survival after out-of-hospital cardiac arrest was greater with active compression-decompression cardiopulmonary resuscitation (CPR) than with standard CPR. In the current study, we assessed the effects of the active compression-decompression method on one-year survival. METHODS: Patients who had cardiac arrest in France, more than 80 percent of whom had asystole, were assigned to receive either standard CPR (377 patients) or active compression-decompression CPR (373 patients) according to whether their arrest occurred on an even or odd day of the month, respectively. The primary end point was survival at one year. The rate of survival to hospital discharge without neurologic impairment and the neurologic outcome were secondary end points. RESULTS: Both the rate of hospital discharge without neurologic impairment (6 percent vs. 2 percent, P=0.01) and the one-year survival rate (5 percent vs. 2 percent, P=0.03) were significantly higher among patients who received active compression-decompression CPR than among those who received standard CPR.

Chest. 1994 ;106:872-9. Survival after in-hospital cardiopulmonary arrest of noncritically ill patients. A prospective study. Berger R, Kelley M. Veterans Affairs Medical Center, Lexington, KY 40511.
BACKGROUND: The rising healthcare costs and the ethical and economic implications of cardiopulmonary resuscitation (CPR) have generated interest in defining criteria to predict the appropriateness of CPR in specific patients. Age has been proposed as one such a criterion. METHODS: As part of a quality assurance program, all instances of CPR (code-500) at our VA Medical Center were prospectively studied over a period of 45 months. Only events in noncritical care hospital areas were included in this analysis. The CPR data were prospectively collected, and follow-up of initial survivors was continued until the end of the study period or until a patient died. RESULTS: Of a total of 422 code-500 events, 387 (92 percent) met our study definition of cardiorespiratory arrest, and 255 of these occurred in a noncritical care area and were included in the study. Our immediate survival was 52 percent (n = 132), survival after intensive care unit (ICU) stay was 22 percent (n = 55), survival to hospital discharge was 11 percent (n = 28), and 4 percent of the patients (n = 10) were alive at the end of follow-up (mean, 22 months). None of the patients discharged alive had a significant new neurologic deficit, and all but one returned to their preadmission environment. The post-CPR hospital charges for each of the surviving patients was estimated at $63,000. Whether in-hospital CPR in noncritical care areas is cost-effective is an issue that society at large must eventually decide.

Drugs Exp Clin Res. 1992;18:355-65. Controlled study on L-carnitine therapeutic efficacy in post-infarction. Davini P, ea Santa Chiara Hospital,Pisa, Italy. A controlled study was carried out on 160 patients of both sexes (age between 39 and 86 years) discharged from the Cardiology Department of the Santa Chiara Hospital, Pisa, with a diagnosis of recent myocardial infarction. L-carnitine was randomly administered to 81 patients at an oral dose of g 4/die for 12 months, in addition to the pharmacological treatment generally used. For the whole period of 12 months, these patients showed, in comparison with the controls, an improvement in heart rate (p < 0.005), systolic arterial pressure (p < 0.005) and diastolic arterial pressure (NS); a decrease of anginal attacks (p < 0.005), of rhythm disorders (NS) and of clinical signs of impaired myocardial contractility (NS), and a clear improvement in the lipid pattern (p < 0.005). The above changes were accompanied by 90% lower mortality in the treated group (1.2%, p < 0.005), – in the control group mortality was 12.5%. Furthermore, in the control group there was a definite prevalence of deaths caused by reinfarction and sudden death. On the basis of these results, it is concluded that L-carnitine represents an effective treatment in post-infarction ischaemic cardiopathy, since it can improve the clinical evolution of this pathological condition as well as the patient’s quality of life and life expectancy.

Mol Aspects Med. 1994;15 Suppl:s165-75.
Usefulness of coenzyme Q10 in clinical cardiology: a long-term study.Langsjoen H, University of Texas Galveston .
Over an eight year period (1985-1993), we treated 424 patients with various forms of cardiovascular disease by adding coenzyme Q10 (CoQ10) to their medical regimens. Doses of CoQ10 ranged from 75 to 600 mg/day by mouth (average 242 mg). Patients were followed for an average of 17.8 months, with a total accumulation of 632 patient years. Eleven patients were omitted from this study: 10 due to non-compliance and one who experienced nausea. Eighteen deaths occurred during the study period with 10 attributable to cardiac causes.. Of 424 patients, 58 per cent improved by one NYHA class, 28% by two classes and 1.2% by three classes. A statistically significant improvement in myocardial function was documented . Before treatment with CoQ10, most patients were taking from one to five cardiac medications. During this study, overall medication requirements dropped considerably: 43% stopped between one and three drugs. Only 6% of the patients required the addition of one drug. No apparent side effects from CoQ10 treatment were noted other than a single case of transient nausea. In conclusion, CoQ10 is a safe and effective adjunctive treatment for a broad range of cardiovascular diseases, producing gratifying clinical responses while easing the medical and financial burden of multidrug therapy.

Mol Aspects Med. 1994;15 Suppl:s143-7. Coenzyme Q10 and antioxidants in acute myocardial infarction.
Kuklinski B, ea Klinikum Südstadt, Rostock, Germany.
Sixty-one patients admitted with acute myocardial infarction, and a symptom’s duration of less than 6 hr were randomized into two groups. Immediately after hospitalisation, members of the verum group (n = 32) received 500 mcg of selenium (as sodium selenite). Thereafter they received a daily dosage of 100 mg coenzyme Q10 (Bio-Quinone) and 100 mcg selenium (seleno-methionine) for a period of one year. The control group (n = 29) were given matching placebo preparations.. Biochemical parameters showed a reduced concentration of CPK- and ASAT-level in the verum group during the acute phase (although not statistically significant). None of the patients in the verum group (i.e. on antioxidative treatment) showed prolongation of the frequency corrected QT-interval. In the control group, 40% revealed a prolongation of the QT-interval by more than 440 msec (p < 0.001). There were no significant differences, with respect to early complications. During the one-year follow-up period after myocardial infarction, six patients (20%) from the control group died from re-infarction whereas one patient from the verum group suffered a non-cardiac death.

Int J Tissue React. 1990;12(3):163-8. Pronounced increase of survival of patients with cardiomyopathy when treated with coenzyme Q10 and conventional therapy. Langsjoen PH, ea Scott and White Clinic, Temple, TX USA.
During 1982-86, 43/137 patients with cardiomyopathy, Classes II, III and IV, had ejection fractions (EF) below 40%, and a mean EF of 25.1 +/- 10.3%. During treatment of these 43 patients with coenzyme Q10 (CoQ10), EF increased to 41.6 +/- 14.3% (p less than 0.001) over a mean period of 3 months (range, 2-4 months). The mean CoQ10 control blood level was 0.85 +/- 0.26 micrograms/ml which increased on treatment to 1.7 to 2.3 micrograms/ml for five periods up to 36 months (each period, p less than 0.001). The survival rates for all 137 patients treated with CoQ10 and for the 43 patients with EF below 40% were both about 75%/46 months. These two survival rates were comparable between 24 and 46 months, which is of extraordinary significance and importance when compared to survival of about 25%/36 months for 182 patients with EF below 46% on conventional therapy without CoQ10. The improved cardiac function and trippled survival show that therapy with CoQ10 is remarkably beneficial due to correction of CoQ10 deficiency in mechanisms of bioenergetics