Nutrition is becoming increasingly costly as world population mushrooms, and worse, as oil-burning industries immorally pay more  (and governments thus get more in taxes) for plant oil as fuel  than farmers can get for producing food. The hungry poor majority is irrelevant, despite the fact that there has been superabundance of natural  and environmetally friendly power available forever,  and harnessable  by relatively simple technology (which Industry and governments have criminally  suppressed) for decades.

Fish oil omega3 - eicosapentanoic acid EPA and docosahexanoic acid DHA - seems to be the most valuable single nutrition supplement we have, apparently almost halving all major diseases  (and mortality) from brain and immune dysfunction in infants and children to  all the major common degenerative diseases of aging, from vascular and arthritic to immune and mental.

Plant oils have indispensable benefits.  But as people have migrated away from the seaside and fishing, and fish has become scarce so that it is no longer a staple for the poor or as chickenfeed, it is reported that EPA/DHA intake has fallen below 100mg/week in USA. And the more omega6 we eat, and the longer we live, the less EPA+DHA  our metabolism  can apparently make.

So as diet has improved among the better-off on the Food-Pyramid-recommended higher cereal and nut intake, and livestock has been shifted from pasture-fed (at least some omega3) to grain-fed (high omega6), it is estimated that the historical 6:1 ratio of dietary omega6:omega3 in western diet has actually risen adversely to 20:1.

By contrast, historically those who lived as fisher people reputedly had/have the least chronic aging diseases, and the lowest diet omega6:omega3 ratio, reputedly 1:1.

Oils- including  GLA gamma-linoleic acid and ALA alphalinoleic and linolenic acid- are enormously beneficial in humans, especially for immune modulation to steer between hyper immunity - allergy and rheumatic disease- and hypo-immunity - infections and cancer.

But if one eats a prudent Mediterranean-type diet and ensures at least 3gm fish oil i.e. close to a gram of EPA+DHA a day, is it wise or unwise to again increase the already high omega6 excess by encouraging omega6 supplements as in patent products e.g. Effamol?

Most of us older generation were brought up on a spoon of cod liver oil - Scotts Emulsion a day. This custom seems to have fallen into abeyance.

Now it is hard to tell whether this fact - fish oil deficiency - or junk food, or global pollution, or hours of television a day, or the abolition of discipline and obligatory physical exercise at most schools, has contributed more to apparent fall in learning and behaviour achievements in children, and increase in depression, diabetes, overweight, osteoporosis, anxiety, vascular, malignant, inflammatory  and dementing diseases.

There is no evidence that patent mixed fish-plus-plant oils do better than fish oil alone in the indisputable improvement in ADHD attention deficit hyperactivity-disorder in children.

Ross & Henderson’s sentinel (JAMA 1980) paper on the strong relationship between long term oral premarin  total dose and breast cancer was  largely ignored:  that  with cumulative premarin dose >1,500 mg (ie 7yrs) the breast cancer  risk  was estimated to be 2.5 in women with ovaries (vs  0,7 sans ovaries); the risk ratio for a high cumulative dose (ie after about 15years, >3mg premarin)  rose to 5.7 relative to nonusers with normal breasts.

But at the same time, Finnish papers in Maturitas showed why, because of non-physiological high E1>E2 even on oral E2,  systemic ERT is preferred:

Punnonen R ea: (in E2V 2mg/d  & the Renin-Aldost system: 1980:2:91-4) that  “on oral E2v the E2 levels rose to normal and (unlike  on oral premarin, EE2) caused  no rise In BP, aldost, renin; they thus preferred such natural  ERT which does not activate the biliary, RAS renin-angiotensin system, and thrombosis”;

 but Heinonen  PK et al (1982:4: 273-6 Estrogen levels on oral E2) showed that  on E2v  4mg/d orally, blood   E2 rose 5X and  E1 rose 25X; so they recommended avoiding   oral ERT.

Thus the Womens’ Health Initiative confirmed three facts: 

1. starting OHT well after age 60yrs and continuing even modest dose cyclic  (premarin 0.625mg plus MPA 5mg) does more harm than good; THIS SAYS NOTHING ABOUT APPROPRIATE PHYSIOLOGICAL BALANCED COMBINED PARENTERAL TESTOSTERONE-PROGESTERONE-ESTRADIOL HRT FROM ANY POSTMENOPAUSAL AGE HAVING ANY  LIFELONG RISKS WHATSOEVER.

2. starting the same OHT regime soon after menopause - especially premarin alone- reduces  all major diseases and mortality by about a third, except for rare cases of deep vein thrombosis and cholelithiasis;  this outcome was confirmed in the 9year RCT in Finland (Heikkinen ea 2006) in which women on oral estradiol 1mg/d +- MPA 2.5mg from menopause had zero major adverse events.  BUT THIS SPEAKS ONLY FOR AT MOST THE 9 YEARS THAT  THESE WOMEN WERE IN THE TRIALS.

There are  so far some seven  major functional types of steroid hormones  in humans: calciferols; androgens; estrogens; progestins; glucocorticoids; mineralocorticoids; and  endogenous digitalis- natriuretic hormone (eg Goldstein  2006, Weidemann 2005; Kurup ea 2003) .

     Apart from  gender-reproduction-childhood growth promotion (ie androgens, estrogens & progestins), their actions fall into many other systemic classes; which in conventional “replacement” doses  the literature and experience suggests may be compared as follows:

+=increase;    - = lessen; n = apparently neutral?  AS=anabolic steroids.

The active hydroxycalciferols are in a sense exocrine ie are produced from ingested  vitamin D3 and cholesterol in the skin and kidneys, not from dedicated endocrine glands; but while their synthesis needs no more than an hour of sunlight a week in sunny climates, and modest kidney function, calciferol deficiency is increasingly recognized in those who take little dairy products, and little sunshine. Thus the pituitary, skin,  parathyroids, adrenals  and  gonads are the primary  endocrine glands of growth.

The other steroid hormones (like the other major anabolic hormones- insulin and human growth hormone HGH) are endocrine ie are vulnerable to both intrinsic endocrine failure (Hypothalamic-Pituitary-Adrenal- pancreatic-Gonadal ),  and to  endocrine gland decrease and blockage by infections, cancer, major stress, auto-antibodies or direct trauma.

       All these anabolic  hormones  if swallowed are destroyed  by digestion/  1^st-pass hepatic metabolism; thus to achieve the same systemic effect,   comparative doses are reported as follows:                 

The vulnerability  of oral steroid therapy is illustrated by oral contraception: where taking eg an oral antibiotic can compete for absorption, reducing   blood SH levels so that accidental conception occurs. Similarly, a postmenopausal  patient with rheumatoid arthritis, on oral (E+P HRT), reports that  her analgesic  requirements  rise while she is on antibiotics.

     One  needs to go back to a standard textbook of Pharmacology of  1958, (Kranz & Carr: Pharmacological Principles of Medical Practice: Balliere, London) to find the corollary:  eg “cortisone acetate implant, or im  2-5mg daily injection as replacement for  Addisons’ Syndrome”: “For menopausal symptoms, combined E+TT is often employed…”;  “oral synthetic estrogens (have replaced natural ones due to availability,  oral form & lower cost; but) produce undesirable: nausea, cramps, migraine and male breasts.    Estrogen + TT are additive, and E doses may therefore be reduced   since the combination gives smoother transition:  73% of patients remain  symptom free.    TT 10mg imi 3 x/week may control  functional uterine bleeding better than progesterone”!.

      It is widely overlooked that  TT is converted irreversibly by aromatase to E2 in the tissues; but   giving E2 does not do the reverse – it  suppresses the  HPAG and   TT production. Thus women need to be given TT with estrogen, but  men do not need to be given estrogen -  giving them TT increases their E2 levels by about 1/3. This source of E2 may not be enough for balance in women, but reduces their needed dose of administered estrogen;  hence in women  on a standard 20:1 TT:E2  injection combination, or on combined implants eg TT 50mg + E2  20mg/6months,  the blood TT level should be monitored to check that the mean TT is in the physiological range of  1-3.5nmol/L, but the E2 level need  not be above perhaps 0.1nmol/L – in fact, to avoid excess fat deposition and breast cancer stimulation, it must  not , since TT is supplying E2 direct in target organs.

     Hence Ginsberg J & Prevelic GM  at Royal Free Medical School  ( Drug Therapy & Reproductive Endocrinology: London: Arnold 1996) note that in BRCA, androgen + prednisone give good results;  they advise: parenteral> oral ERT: eg  E2 patch 50u/d;  or Implants eg TT 50mg + 20mg E2 /6mo (= 300mcg TT + 110mcg E2/ day)..

In TOPICS IN O & G 1998: (ed Julian Bassin: Julmar Communications, Jbg 4^th Ed 1998: sponsored by all the RSA gyne Drug Suppliers):  Schnitzler CM wrote that “ERT should be given for life, from as early as possible, but even from 80yrs; the elderly not exposed to the sun needing >2000u vit D/day. Sonnendeker on HRT wrote that oral  HRT raises both coagulation & renin substrates acutely; EE2 should not be used for ERT; thus he prefers oral ERT except  if coagulopathy, liver/biliary/ triglyceride/ or vascular headache  problems, when he uses non-oral ERT. Indications for androgens are: poor libido; persistent tiredness & OP; preferring the 25mg TT pellet to oral androgens or imi esters”.

Finally, the physiological logic of parenteral  (as opposed to oral) HRT- in this case sex hormone replacement) was already well recognized and marketed over 60 years ago – even in South Africa- in eg the handbook Sex Endocrinology (Schering, New Jersey, 1944) which recommended and listed creams, injections and implants as well as tablets.

William Masters and colleagues followed this up with the first apparent RCT of HRT published in 1953,  who showing  in a 13month titration RCT that biweekly ie shortacting  esters  imi TT 20mg  + E2 1mg    (= T ~2.8mg/d + E2 ~0.14mg/d, ie a ratio of 20:1 to 22:1 – as in Schering’s Primodian Depot or Organon’s Mixogen)  restored 70% of geriatric women in their mid70s to selfcare; allowing the nursing staff on the unit to be halved. Overall the women had ~one brief menstrual bleed  after about 5weeks, thereafter on follow-up biopsy all maintained endometrial atrophy. Some  needed initial T:E dose titration (between eg 30:1 to 15:1)  for individual variation in response. As a result  both Schering and Organon to this day sell this preparation as a 100mg TT ester + 5mg estradiol ester ial, to be given as desired every 3 – 6 weeks.

     We have found for the past  ~10 years that, just as hypogonadal men do optimally  on about 200mg depotrone subcutaneously sc  every fortnight (= 10mg TT a day), women do well on  Masters’  20:1  TT:E2 hormone ratio, the optimal regime being on average 0.2ml 20mg of hormones by domestic  subcutaneous selfinjection every 2 weeks ie TT 1mg/day and E2  0.05mg/day,  – the average resultant  blood levels being TT round 2.5nmol/L - but of course the testosterone itself delivering far more estradiol extra- and intracellularly.

  With this regime we have never seen a breakthrough bleed in postmenopausal women, for the simple reason that follow-up endometrial ultrasound uniformly shows endometrial atrophy. We have also never seen increasing changes on follow-up screening mammography since it is common cause that testosterone suppresses female glandular breast proliferation.  

These  results with arenteral HRT  have been abundantly confirmed in women followed for up to  40years on parenteral HRT by leading menopause clinics such as Greenblat  & Ganbrell(Augusta); Gelfand(Montreal); Schiff(Boston), Buster(Houston), Notelovitz (Florida), Vliet(Tucson), Lichten(Michigan), Shippen(Philadelphia), Karpas(Atlanta); Schleyer-Saunders, Whitehead and Studd(London UK); Tvedegard Moller & Hansen(Copenhagen); Burger & Davis, Zhou & Dimitrikakis (Australia); and our Cape Town group under Davey;

and

most important of all:  since longterm trials beyond the necessary critical 20 years  will never be carried out in humans due to the cost, the results of primate studies by Thomas Clarkson ea at Wake  Forrest University  showing  that starting even oral premarin at castration in young  female monkeys and continuing it for the human equivalent of 15 years blocked onset of atheromatous disease ; but premarin alone or with MPA  produced breast proliferation;  but like endometrial proliferation, this was suppressed by testosterone replacement.

       The greatest myth (if not drug industry  hoax) of the past 30 years may be the claim that postmenopausal women (or for that matter women needing contraception) need a patent estrogen and a synthetic progestin for endometrial  and breast protection and contraception; when it was shown decades ago that depot estradiol plus depot progesterone- or better still,  depot estradiol plus depot  testosterone plus depot progesterone - do best for both contraception and HRT  and all-system protection against all the degenerative diseases of aging. 

The fevent hope and effort  of the patent designer drug industry is that they can buy off enough practitioners, academics, researchers, Regulators and politicians so that the widespread avilability, low cost - and massive all-disease prevention- of such natural supplements as human hormones as well as the dozens of other proven biologicals including vitamins and mineral is never appreciated and utiized. They cannot curb their insatiable lust   for immediate endless profits no matter how much suffering it causes - disaster capitalsm- by recognizing that if they now promote such safe cheap proven panaceas to both the poor and the prosperous consumers, they will extend healthspan by decades, producing far more survivors who will later rather than sooner still need/want to buy their designer products.

4. to follow: THE IMPORTANCE OF THE SITE OF PARENTERAL INJECTIONS

See Drs Jeff Dach / Leonard Berlin’s comments on screening mammography.

http://www.jeffreydach.com | jdach@bellsouth.net | 65.2.47.69

Limitations of Screening Mammography

An eminent radiologist, Leonard Berlin MD says we have failed to disclose the limitations of screening mammography, namely that mammography will miss 30-70% of breast cancers, and leads to over diagnosis and over treatment.

Dr. Berlin says disclosures of these limitations should be mandated, just like the cigarette and drug warnings that appear on their ads.

Dr. Berlin also points out that 57% of the American women believe that mammograms prevent breast cancer, a misleading message from Breast Awareness Month.

Mammograms are designed to detect cancer, not prevent it. Thinking that a mammogram can prevent breast cancer is like thinking that checking your house annually for broken windows prevents robberies.

To read more: http://jeffreydach.com/2007/11/04/the-untold-message-of-breast-cancer-awareness-month.aspx

The Untold Message of Breast Cancer Awareness Month by Jeffrey Dach MD

Jeffrey Dach MD
4700 Sheridan Suite T
Hollywood Fl 33021
954 983 1443
http://www.drdach.com
http://www.jeffreydach.com
http://www.naturalmedicine101.com

In chapter 1 we examined the importance of the blood measurement of HRT - hormone replacement.

This chapter 2 reviews the evidence for the importance of the source, the origin of HRT.

The textbook WOMENS’ BODIES, WOMENS’ WISDOM by ObGyn Prof Christiane Northrup (2nd Ed Piatkus UK 199 is the only book found which details “the source of all marketed sex hormones”: which at that time, was -
i) EQUINE : MARES’ URINE for Wyeth-Ayerst’s Premarin estrogens;
But “all other prescribed sex hormones are derived from
ii) PLANTS -yams and soya:
the Estrogens - estradiol, estrone, estriol, mestrone, diestranol;
the Progestins - progesterone; norethisterone & dydrogestone;
Testosterone - implants, Sustanon and all the TT esters; and
Tibolone - a weak synthetic estrogen-progestin-androgen:”
(to which RSA has added the African potato/yam for: Moducare); except
iii) SYNTHETICS: the (progestins) levonorgestrol & medroxyprogesterone were
the exceptions, listed as being ‘synthetic’ ie presumably laboratory synthetised.

In April 2008 Northrup reasserts the primacy of for-survival mother Nature’s optimally evolved bioidentical hormones over the 50 year old xenohormones including synthetics - of for-profit Father pharmaceuticsl like Wyeth. see link http://www.drnorthrup.com/news/bioidentical_hormones.php

But (other than E2, TT, DHEA & progesterone) we cannot ROUTINELY measure the dozens of SH which HT (ie other than human estradiol, testosterone, progesterone, DHEA) eg premarin, progestins produce in the blood - estrone, estriol; ethinylestradiol; equilins; progestins; or anabolic steroids; - whether these derive from mares’ urine, soya, yam, African potato, black cohosh or laboratory synthetics.
Thus it is not THE ORIGIN of SHR WHICH MATTERS, BUT WHETHER it (HRT) gives PRIME hormones ( DHEA, TT, E2, progesterone), MEASURABLE IN THE PATIENTS’ BLOOD.

As Dr Lee Vliet points out in SCREAMING TO BE HEARD (Evans, New York, 2001), “Conjugated estrogens eg Premarin is only 0.5% measurable E2 estradiol; the other 99.5% we cannot routinely measure: 50% is estrone, the rest is scores of other horse estrogens not found in humans”, ie not routinely measurable.
So women are urged by Wyeth, and allowed by the FDA, to take a potent pregnant-mare based compound which ensures some measurable estradiol level, but also ensures potent estrogens at more than hundredfold the bloodlevel of the optimal physiological estradiol level. No wonder oral premarin promotes major complications early in most women, and lifethreatening if continued for more than a dozen years. Why do Regulators (eg the FDA) allow this, except for massive profits for the Regulator, the fiscus, and Industry- Wyeth which creates many jobs, and the Disease Industry that has to take care of the increasing complications of the premarins?

As Vliet’s graphs show, “systemically administered E2 is the ONLY estrogen which raises predominantly the plasma E2 level – the prime youthful estrogen; as opposed to all other (and inferior ) estrogens, which compete with E2 for the estrogen receptor ERs. Premarin especially binds tightly to the ERs”, suppressing and blocking what little E2 older women get or make.

Arising from eg Vliet, there are some six emotive issues to be distinguished in all HRT:
(i) While humans are omnivorous, few usually drink even their own urine, let alone milk, meat or urine from pregnant mares; drinking urine as medicine is condemned by allopathic medicine.
(ii) Thousands of mares across North America are kept pregnant, permanently catheterized,
sedated, tethered to collect their gallons of urine which only Wyeth may (presumably by patent) use (@>$17/liter) to extract Premarin;
(iii) Because of the risk of allergy and eg prion (BSE) infection transmission let alone HIV and newer infections, animals are no longer used as SOURCE of ANY HRT except Premarin; (salmon calcitonin may still be a rare exception). Medicinal products derived even from man (from blood or organs) regularly cause immune or infection disaster..
(iv) Premarin is the only HRT in common use which reportedly has still not been fully characterised – hence Wyeth, via the FDA, has for 50 years deviously prevented any other manufacturer from registering a generic! It is said that at least 40 different steroids have been detected in Premarin; since these are the breakdown products of horse pregnancy, it is not surprising that (while it reduces symptoms and slows osteoporosis), complex Premarin is badly tolerated and rejected by the majority of women (who do not want to feel pregnant).
(v) Recent major RCTs have failed to show benefit from Premarin in older women with vascular or dementing diseases; and
(vi) Up to 80% of women started on oral HRT –( which in the USA is mostly conjugated Estrogens) – abandon it within 3 years…

Routine animal milk, eggs, meat, and food plant ingestion may all produce allergy and infection when eaten by humans; but provided the hormones synthesized from ANY chemicals are molecularly identical to human hormones, they are human hormones and, if injected without contamination into humans – whether they be insulin, adrenaline, E2, TT, erythropoeitin, granulocyte-stimulating factor, parathormone, growth hormone, chorionic gonadotropic hormone, cortisone or progesterone - cannot cause allergy (unlike eg the synthetic hormone derivative prednisone),..

But Premarin is the sterilized extract of ALL steroid waste products from pregnant mares’ urine, and only about 50% of it’s hormones (E1 and a trace of E2) are identical to human steroids. Other mammals’ meat can produce allergy in humans even when cooked. Hormones surely cannot be cooked or they decompose. Many people are allergic to dairy products; yet women are universally prescribed to drink the product of mares’ urine – and most women abandon it within a few years – wisely so, since the incidence of breast cancer rises steadily with total estrogen dose [Henderson BE , Paganini-Hill A, et al, UCLA: JAMA: 1980;243:1635-9: Menopause, ERT and BRCA 1971-’77 in 138 BRCA cases, most of risk increase was on Premarin in those with ovaries - which make women intolerant of more than low dose ERT.. RR for BRCA for a ERT cumulative dose >1,500 mg(ie 7yrs) was estimated to be 2.5 in women with ovaries vs 0,7 sans ovaries].

To date the FDA - the US Government- sticks piously to it’s defence to the death of Wyeth’s unique right to produce generic premarin since no-one is yet certain of the precise steroid composition of premarin- which the FDA allows to be marketed only by Wyeth although it is long out of patent, and it’s composition (as a biological urine extract) reputedly varies from batch to batch. http://www.fda.gov/CDER/news/cebackground.htm.
It should be noted that the FDA approved Cenestin soy-based “conjugated estrogens CE ” in 1999, now apparently replaced by Barr Pharmaceuticals with Enjuvia, also a plant-derived formulation of 10 synthetic conjugated estrogens http://www.enjuvia.com/patients/about_enjuvia/Default.aspx.

Does it surprise that there are precisely two randomised controlled trials, for 3 -4 months, in 121 women, done in France & USA, published on the clinical benefit of these two (Barr’s) plant-based conjugated estrogens? http://jcp.sagepub.com/cgi/content/abstract/42/3/290.; http://linkinghub.elsevier.com/retrieve/pii/S0378512203002408. American women beware.
But Barrs must be rubbing their hands in glee at the vindication of CE for appropriate use in lower than conventional dose for up to 9 years in the young women in the USA Womens’ Health Initiative (Rossouw ea 2004) RCT.

chapter 3 will examine THE IMPORTANCE OF ROUTE OF HRT?

ndb

Breast

                        · There is a wide variation across the world in the incidence of breast cancer and its risk factors.

                        · There are multiple risk factors for breast cancer, including life-style factors especially alcohol intake, obesity and lack of exercise. These need to be included during counseling to put the magnitude of risk of HRT into perspective [B]

                        · After 5 years’ use of combined estrogen and progestogen, there is a small increase in risk of breast cancer in North American women of about eight extra cases per 10,000 women per year. However, no significant increase was seen in women without prior use of HRT in the WHI study. [A]

                        · Estrogen-only use does not cause an increase in breast cancer for up to 7 years21. [A] In observational studies, a small increase in the risk with estrogen-alone therapy appears with long-term use22. [B]

                        · Women using combined HRT before a diagnosis of breast cancer have a reduced mortality23. [B]

                        · A decline in the incidence of breast cancer in the USA started before the WHI publication and can be partially related to fluctuation in screening. There has been no decline in breast cancer registration in the UK following the Million Women Study report, nor in Norway, Canada, the Netherlands and countries with stable screening programmes25. [B]

                        · Combined estrogen and progestogen therapy may cause increased breast density in up to 50% of postmenopausal women, dependent on the regimen (dosage, type of progestogen). The effect of estrogen alone is smaller26. [A]

                        · The effect on breast density is dose-related. Ultra-low-dose regimes do not cause perceptible change in density[A]

                        · The average increase in breast density under standard-dose HRT is only about 5–10%28. [A]

                        · Increased baseline breast density is a risk factor for breast cancer29. There are no data to support a direct association between HRT-induced breast density changes and the risk of developing breast cancer.

                        · Many women who develop breast cancer have no known risk factors other than growing older. most women with known risk factors do not develop breast cancer.

                        · Individual risk analysis for breast cancer is strongly recommended in clinical practice30.

Bone

 *Overall HRT is effective in preventing all osteoporosis-related fractures even in patients at low risk of fracture[A]

*Although no head-to-head studies have compared HRT to bisphosphonates in terms of fracture reduction, there is

                           no evidence to suggest that bisphosphonates or any other antiresorptive therapy are superior to HRT.

 * It is therefore suggested that, in 50–59-year-old postmenopausal women, HRT is a cost-effective first-line

                                  treatment in the prevention of osteoporotic fractures.

* Even below standard-dose preparations maintain positive influence on bone indices such as BMD[A]

                        · HRT has a positive effect on osteoarthritis and the integrity of intervertebral disks.

Cognition

*At present, there is no evidence of substantial cognitive decline across the menopausal transition[A] However, many women experience cognitive difficulties in association with vasomotor symptoms, sleep disturbances & mood changes.

*Verbal memory performance relates with the objective number of hot flushes women experience but not to the number of hot flushes they report.

*Clinical trials find no cognitive benefit among women initiating HRT late postmenopause (i.e. after age 65).

*Observational studies show a decreased risk of Alzheimer’s disease in hormone users and typically involve women who initiated estrogen therapy early in the menopausal transition. [B]

*Limited data exist on the effect of progestogen added to estrogen in the early postmenopause period. Clinical trial data suggest no cognitive benefit with MPA early in the menopause. [A]

and 7 years since they postulated that statin benefit might be negated long-term by adverse  non- CVD mortality at CVD risk below 1.3%pa.

It is almost 40 years since as a junior medical registrar I was first advised to take lipid-lowering drugs (clofibrate- just a few years before the cancer link came out),

and  have since then been advised  to take statins .

I have never done so  (for my familial mild-moderate type 2b  lipidemia),  because the evidence has never justified such experimental and long-term unproven synthetics (as with modern antidiabetic and anti-osteoporotic wannabe money spinners) in search of $billions for the western Drug Corporations and their investors and lobbyists.  

   Lately,  despite the massive statin trials, the last  statin  metanalysis (2003 from University Slovenia) again failed to show any reduction in non-CVD cardiovascular  disease mortality;

and since CVD is the major cause of death and disability  ONLY in those who already have such disease, statins remain indicated only in secondary prevention -as was shown in the last two major trials published, in 2002 ( ALLHAT-LLT  and WESCOPS), now confirmed in the Japanese MEGA study  (2006) of low dose statin, which (in primary prevention in a slim population)  showed similar barely significant 1/3 CVD mortality benefit- significant reduction only in myocardial infarction -  but no significant other  cardiovascular or non-vascular benefit even after a mean of 5.3years, 41 000 patient-years.   

 Last month  Theo Jacobson from Emory University in Atlanta GA  commented that myalgia is the leading reason why patients abandon statins. 

 In 2000 he already questioned the marketing hype for statins  that “the lower the cholesterol level is driven, the better” . 

The growing scandal is the increasing marketing  pressure  by Big Pharma lobbyists (including  some Regulator  staff) to promote prescription and even over-the-counter use of statins to achieve ever-lower low-density lipoprotein levels even in the absence of any vascular disease or CVD risks- including the farcical inclusion of statin in a PolyPill (led by Ward and Law and the BMJ in  UK). .

 Last year Kilmer McCully himself  (the father of the homocysteine hypothesis in CVD 1969) points out that the dramatic fall in CVD mortality  since  it’s USA peak in 1955 correlates well with voluntary and mandatory fortification with B6, B9 and B12 (let alone niacin) .

We may also note that  falling  premature CVD mortality coincides with

• the increasing use of metformin the past decades  (which lowers all-cause morbidity and mortality, and new diabetes, by 1/3,  and overweight by about 8%); for both treatment and prevention of type 2 diabetes, overweight, lipidemia and polycystic ovary syndrome.;
• and with increasing use of appropriate sex hormone replacement for aging men and women (which lowers all-cause morbidity and mortality by 1/3); .
•  and with targeting of lower blood pressure levels even in the elderly hypertensives since the SHEP trial (1985).   
•  and with growing intake of supplementary fish oil ((which lowers all-cause morbidity and mortality by  almost 1/2);  
•   and  of other insulin sensitizer- Nitrric oxide - antioxidant -metabolic promoters  (like vitamins A,  B1, B3,B7, C, D, E, K, calmag, zinc, chromium and other trace elements), and the dozens of our other  crucial  biologicals that decline with aging and illness, (like coQ10, n-acetyl cysteine, arginine, carnitine, carnosine, ribose, chondroglucosamine, lipoic acid, taurine, bioflavinoid, thyroid, melatonin  etc).

And while statins have legion adverse effect from insidious fatigue to myositis and hepatorenal impairment; dermatitis, depression; reducing steroid levels and virility; and lately  producing even lung damage, (unlike the natural supplements listed  that are the best drugs),  they have never been shown to have the slightest benefit on non-CVD pathology, from overweight and insulin resistance - diabetes  to arthritis. Manufacturers and lobbyists have studiously avoided head-on trial comparison with  the natural CVD preventatives  listed above which simutaneously address both the underlying metabolic cause of hypercholesterolemia (insulin resistance and atheroma) and all the other major common degenerative diseases of aging. So the direct highpressure marketing od statins to the public  - without prescription - for other than severe resistant hypercholesterolemia is thus dangerous massive corporate fraud.

So there is every reason why statin use should be severely limited to only  high-risk CVD cases i.e. those with  dangerous homozygous familial hypercholesterolemia resistant to all other  interventions.

see for references: