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Holistic Lifestyle Counseling

Statins Exposed

This Journal presents a raft of information on statins and why statins are not such a great drug after all. The common use of statin drugs is based on a faulty model of how atherosclerosis develops.

The use of statins should be approached with discernment, discrimination, and some caution. There is a place for statin usage in those who are not willing to incorporate healthy lifestyle practices; namely, eating whole foods, physical exercise, stress reduction, and developing sound sleep practices. While you are working on improving these aspects of your life, you should also consider the health of your relationships.

The collation of information presented here is from Dr. James Roach, M.D., who is over in Midway, Kentucky. He puts out a very informative monthly email collection of articles about developing health by more natural means. It’s mostly a lot of common sense considerations which this indefatigable doctor backs up with voluminous credible articles from various medical and health journals.

I recommend Dr. Roach’s monthly research offerings which you can view and sign up for here…The Midway Center for Integrative Health.

For what it may be worth, I wrote about some of this back in 2013 in this Journal…The New Cholesterol Guidelines.

A healthy level of cholesterol is very important for our health. Cholesterol is a main component of all cell membrane structures. Approximately 30% of the brain is cholesterol as the main component of much of the nerve structure make-up. Cholesterol is also the molecule that all sex hormones are made from…pregnenolone, progesterone, DHEA, estrogen, testosterone, and cortisol.

Physicians who prescribe statin drugs often seek to lower their patients’ cholesterol levels to around 140-170 mg/dL, which I consider to be too low for cellular health. If you are taking statins and your total cholesterol is less than 170 you should rethink this approach while considering the known facts about how it is that blood vessel disease develops.

The 2 Journals on Blood Vessel Health, Part I and Part II reveal more information about cholesterol and its involvement in the pathology of blood vessels. The causes of atherosclerosis are covered in these writings, and the role of cholesterol in arterial narrowing is explained.

Also, I recommend this summary writing by The Midwestern Doctor, whose writings are always well researched and composed. Please see Statins, Cholesterol and the Real Cause of Heart Disease. The full writing of this article can be read here.

I made little attempt to edit the appearance of Dr. Roach’s excellent and exhaustive research collection on statins and cholesterol, presented below.

Have a look!

 

Statins
**Most studies of LDL and risk of all cause mortality have found no association[i],[ii],[iii] or an inverse association[iv],[v],[vi] **

Though I personally strive to get all my patients off statin cholesterol medicine, it is essential that safe, appropriate strategies to replace the Rx medicines be utilized under trusted holistic health provider guidance with regular monitoring of D-dimer, fibrinogen, C-reactive protein, and periodic monitoring of homocysteine, testosterone, and vitamin D. We have had excellent success at preventing cardiovascular events using this approach.

Potential side effects of statin cholesterol medicine (many side effects are common); many references are at the end of the handout:

  1. ***Caused COGNITIVE IMPAIRMENT in 75%***
    1. This was reversible in 90%. Pharmacotherapy. 2009 Jul ;29(7):800-11
    2. The relative risk of acute memory loss in the first 30 days of statin use was 4.4-fold higher vs. not on cholesterol medicine. JAMA Internal Medicine 6/2015
    3. Clinically in our office they are a leading cause of Alzheimer’s dementia
    4. While statins can reduce vascular brain damage…
      1. The brain is 70% fat, 53% cholesterol; therefore, would shrink the brain
  2. ***The #1 CAUSE OF NEUROPATHY***
    1. Associated with a 16-fold increase in polyneuropathy, and 26-fold increased risk if on a statin for 2 years. Neurology. 2002 May 14 PMID: 12011277                
      1. Incidentally, the brain is composed of nerves
    2. Diabetes is conventionally considered the #1 cause of neuropathy
      1. In my diabetic patients with neuropathy, essentially all are on statins
      2. WHEN I STOP THE STATIN…
        1. THE NEUROPATHY TYPICALLY IMPROVES WITHIN DAYS
    3. Simvastatin inhibited central nervous system remyelination by blocking progenitor differentiation Am J Pathol. 2009 May;174(5):1880-90.
    4. AT LEAST 88 OTHERS STUDIES FURTHER LINK STATINS TO NEUROTOXICITY (nerve damage), including 12 studies on statin-induced peripheral neuropathy. GreenMedInfo (see end of this handout to click on the specific studies)
  3. #1 CAUSE OF DISABILITY? 
    1. In 2021 54% of the U.S. had disorders affecting impacting nervous system health and were the top cause of disability. Most prevalent: tension-type headache (121.9 million), migraine (57.7 million), and diabetic neuropathy (17.1 million). Conditions with the greatest collective disability were stroke (3.9 million DALYs), Alzheimer and other dementias (3.3 million DALYs), diabetic neuropathy (2.2 million DALYs), and migraine (2.1 million DALYs) (As I have found statins to be the #1 cause of neuropathy and 1/3rd of American adults are on statins, statins are likely the #1 cause of disability-JR).JAMA Neurol Nov 24, 2025 doi: 10.1001/jamaneurol.2025.4470
  4. AS HORMONES ARE ANABOLIC (building, strengthening), STATINS, by LOWERING HORMONES, ARE CATABOLIC meaning EVERY ORGAN, TISSUE, and CELL IN THE BODY IS ATROPHIED BY LOW HORMONES including the BRAIN in my experience
  5. Statins LOWER TESTOSTERONE (20% in my male patients)
    1. Free testosterone levels were higher before statin therapy, obviously decreased after six months of statin therapy, and subsequently increased six months after discontinuing statin therapy (22.4±3.1ng/ml vs. 20.9±2.8ng/ml vs. 22.6. Diabetes Res Clin Pract. 2016 Oct;120:81-8. doi: 10.1016/j.diabres.2016.07.026
    2. Lipitor 10mg reduced sperm 31%, vitality 9.5%, motility 7.5%, reduced L-carnitine, morphology; 65% had altered semen even after Lipitor withdrawal
    3. Shrinks testes J Sex Med. Apr 2010 7(4 Pt 1):1547-56. PMID: 20141585
      1. 22% experienced new onset ED. Int J Clin Pract. Feb 2006 Feb PMID: 16451283
      2. ED onset average 62 days (median 29 days); 2.4 fold increase overall, 3.4 fold atorvastatin, 7.1 rosuvastatin Int J Clin Pract. 2006 Feb ;60(2):141-5. PMID: 16451283
  6. As estrogen is made from testosterone, it also should be negatively impacted
  7. TYPE 2 DIABETES increased 87% and MARKEDLY increased incidence of OBESITY; ten-year male VA study J Gen Intern Med 2015 Nov;30(11):1599-610)
    1. OBESITY increased 82% in those initiating blood pressure or lipid-lowering Rx medicine, and physically inactive 8%.Feb 5, 2020 J Am Heart Assn https://doi.org/10.1161/JAHA.119.014168
    2. MICROSCOPIC ALBUMINURIA 101% more likely on statins. Diabetics had 92% higher risk, smoking 49%. PLoS One. Feb 16 2012 ;7(2):e31639. PMID: 22359611
  8. Promote arteriosclerosis (CALCIFICATION of arteries) by lowering vitamin K
    1. Associated with a 52% increased prevalence and extent of coronary artery plaques containing calcium. Atherosclerosis. 2012 Aug 24 PMID: 22981406
    2. Associated with increased coronary artery and aortic calcification in diabetics and severe atherosclerosis. Aug. 8th, 2012 Diabetes Care
    3. Do not slow progression of coronary artery calcium scores
  9. CARDIOVASCULAR
    1. Does Hypertension worsen? (it lowers powerful blood pressure lowering CoQ10)
    2. A secondary analysis of SPARCL found no difference in effect of atorvastatin in reducing strokes or cardiovascular events in subjects with or without type 2 diabetes or metabolic syndrome.
    3. Stroke recurrence occurred similarly in high-intensity statin and moderate-intensity statin groups (3 months: trend of 12% increased risk, 12 months 8%. High-intensity statins were linked to an 86% increased risk of INTRACRANIAL HEMORRHAGE at 12 months (safer, better strategies are much preferred-JR). J Am Heart Assoc. 2024;13:e035337. DOI: 10.1161/JAHA.124.035337
      1. High‐intensity statins were associated with an 81% increased risk of intracranial hemorrhage at 3 months
  10. An instantly fatal intra-cerebral hemorrhage killed the publisher of my first book who was on a statin
  11. Even a review of conventional research in BMJ showed statins add only 3 days to life expectancy – 4 days over 5 years in those with cardiovascular disease over 5 years (this is without looking at all the side effects that increase mortality-JR)
  12. Evidence does not show a cardiovascular risk benefit to giving heart patients higher doses of statins to drive their moderate LDL down to the 70 mg/dL range. Reaching 100mg/dl is sufficient. 6-2016 JAMA Intern Medicine
  13. No study has shown an impact of statins on cardiovascular outcomes among older adults without preexisting coronary disease or significant risk factors
  14. Number needed to treat to prevent 1 atherosclerotic cardiovascular disease using moderate-intensity and high-intensity statin therapy, respectively, was 32 and 21 for CCS criteria, 30 and 20 for ACC/AHA criteria, 30 and 20 for NICE criteria, 27 and 18 for USPSTF criteria, and 29 and 20 for ESC/EAS criteria. JAMA Cardiol. 2019;4(11):1131-1138. doi:10.1001/jamacardio.2019.3665
    1. Patients with middle HDL, not higher HDL, showed the greatest freedom from major adverse cardiovascular events
  15. Women with the lowest LDL were 2.2 times more likely to have a bleeding stroke as those with high LDL
  16. Coronary artery disease with HDL-C levels >80 mg/dL had a 96% higher risk of all-cause mortality and a 71% higher risk of cardiovascular mortality
  17. Statin trials in the elderly (PROSPER), in patients with heart failure (CORONA, GISSI-HF), and in patients with renal failure (4D, AURORA, SHARP) have all failed to demonstrate a mortality benefit
  18. Centenarians that have higher than normal cholesterol are in better condition, both physical and cognitive 
    1. They had higher blood pressure, total cholesterol, and HDL
      1. HEART FAILURE: 6.7 million Americans have heart failure (HF) accounting for 45% of heart-related deaths. 1 in 4 Americans will have HF in their lifetime if action is not taken to reverse trends (heart failure is RARE AT OUR OFFICE, indicating this is virtually always preventable; STATINS WEAKEN HEART MUSCLE by lowering testosterone and CoQ10-JR).  10-25 Journal of Cardiac Failure.
  19. Statins associated with a 30-36% higher prevalence of KIDNEY DISEASE
  20. Induced DEFICIENCIES – these nutrients are crucial
    1. CoQ10, vits B3, D, E (tocopherols, tocotrienols), K, heme A, omega-3 fats, magnesium, selenium, copper, zinc, iron, carnitine, creatine, glutathione, iodine, phosphatidylcholine
  21. Statins are MITOCHONDRIAL TOXINS-CoQ10: integral for mitochondria/cell energy
    1. CoQ10 levels drop 40% J Clin Pharmacol. 1993 Mar;33(3):226-9.
    2. Creatine, carnitine, selenium, magnesium, vitamin D, K, B3, glutathione, and omega-3 fat deficiencies WORSEN mitochondria
    3. Every cell in the body is worsened
    4. CoQ10 deficiency present in ‘Multiple Systems Atrophy’ affecting moving and involuntary bodily functions
  22. Reduces GLUTATHIONE – the main detoxifying nutrient substrate
  23. Raises HOMOCYSTEINE, a broad marker for higher disease risk across the board through impaired detoxification
  24. Lowers CORTISOL which hurts stress response. Horm Metab Res. 2020 Oct;52(10):742-746. doi: 10.1055/a-1099-9556.
  25. INHIBITS THE IMMUNE SYSTEM increasing infection risk, reduces lymphocytes and viral defense; testosterone deficiency reduces bone marrow white cell production
  26. BRAIN ADVERSE EFFECTS via a slew of nutrient and hormone deficiencies
    1. Parkinson’s disease
    2. ALS (amyotrophic lateral sclerosis), ALS-like syndrome
    3. Transient global amnesia – the primary cause is statins
    4. Personality changes can occur
    5. Impairs thinking
    6. Depression suggested in some studies
    7. Anxiety
    8. Hostility and aggression – 2 of 6 studies showed increased risk
    9. Paranoia
      1. Aggression
      2. Sleeping disorders  Tidsskr Nor Laegeforen. 1997 Sep 20 ;117(22):3210 PMID: 9411859
      3. 54% of U.S. had disorders impacting nervous system health – the top cause of disability (so statins may be #1 cause of disability-JR). JAMA Neurol Nov 24, 2025 doi: 10.1001/jamaneurol.2025.4470
    10. HEARING LOSS
      1. 60% greater risk, 36% tinnitus. Ann Otol Rhinol Laryngol. 2026 Jan;135(1):20-26. doi: 10.1177/00034894251359135
      2. 41%-72% of type 2 diabetics had a higher risk of hearing loss with higher pure-tone audiometric thresholds across all frequencies, particularly high frequencies (undoubtedly statins are a major part of this due to their severe neuropathy impact-JR). 9-25 Otolaryngology-Head Neck Surgery https://doi.org/10.1002/ohn.1346
  27. CANCER
    1. Linked to a 55% increased risk of PROSTATE CANCER, 86% higher risk with daily use. Chang CC, et al. Prostate. 2011 Dec;71(16):1818-24
    2. Linked to a 74% decreased LIVER CANCER risk, 59% increased PANCREATIC CANCER risk. Sci Rep 14, 2896 (2024). https://doi.org/10.1038/s41598-024-53252-4
      1. 40% higher risk THYROID CANCER Clin Endocr (Oxf). 2014 Jul 30 PMID: 25074346
      2. 23% increased risk colorectal cancer, 29% bladder cancer, 18% lung cancer BMC Cancer. 2011 ;11:409. Epub 2011 Sep 26. PMID: 21943022
      3. Increased incidence of melanoma (50%), non-melanoma skin cancer (60%). Eur J Cancer. 2008 Oct;44(15):2122-32. Epub 2008 Aug 15. PMID: 18707867
      4. Increased risk of cancers of thyroid, esophagus and urinary tract; lung cancer  in women. Pharmacoepidemiol Drug Saf. 2008 Jan;17(1):27-36. PMID: 17944002
      5. Invasive ductal carcinoma (IDC) 83%, invasive lobular carcinoma (ILC) 97%:  In women diagnosed with hypercholesterolemia, current statin users for 10+ years had >double risk of both IDC [odds ratio (OR): 2.04) and ILC (OR: 2.43) Cancer Epidemiol Biomarkers Prev. 2013 Jul 5. Epub 2013 Jul 5. PMID: 23833125
      6. There has been some research suggesting reduced risk of some cancers
  28. OSTEOPOROSIS: statins for 1+ years associated with >3-fold higher risk. 10-2019 Annals of the Rheumatic Diseases
  29. HYPOTHYROIDISM
    1. Iodine deficiency may occur, leading to hypothyroidism
    2. Selenium deficiency impacts selenoproteins affecting glutathione and T4 to T3 i.e. statins can induce hypothyroidism
    3. Reduced conversion of T4 thyroid to T3, the active form of thyroid
    4. Lowers TSH giving the false sense of normal or hyperthyroidism – called ‘pseudohyperthyroidism’
  30. Increased PNEUMONIA risk 150%
    1. Higher LDL actually protected against CHRONIC OBSTRUCTIVE LUNG DISEASE
    2. Lowers CREATINE, reducing muscle, vitality, brain function, and straining methylation (think ‘MTHFR’) which impairs detoxification, DNA repair, and many other key functions
  31. Acute KIDNEY FAILURE requiring hospitalization increases 34% in high dose statins
  32. PREGNANCY CATEGORY X (it causes serious birth defects and should never be used by a woman who is pregnant or planning pregnancy
  33. ANEMIA risk 62% higher
  34. EYE COMPLICATIONS
    1. Cataracts, double vision, drooping eyelid, impaired eye motion
    2. In those over 39, statins were associated with a 13% higher glaucoma prevalence, in those over 59, prevalence was 28% higher. Aug 2024 Opthamology Glaucoma
    3. 1.8% on statins reported eye events; 48.4% blurred vision, 25.7% visual impairment. Int J Clin Pharm. 2015 Oct doi: 10.1007/s11096-015-0128-x
    4. Acute macular disease increased 19% and 30% respectively on ACE inhibitor blood pressure medicine or statins Curr Drug Saf. 2008 Jan PMID: 18690977
      1. Case report: a 51 yo woman developed persistent headache, blurred vision, and diplopia (double vision) shortly after initiating atorvastatin. These recurred when switched to rosuvastatin and lovastatin. All symptoms resolved completely after permanent discontinuation of statins, (as atorvastatin is fat soluble, it has the worst impact on brain and nerves-JR)Clin Med Insights Case Rep Dec 2025 10;18:11795476251400972. doi: 10.1177/11795476251400972
  35. MUSCLE
    1. Muscle weakness from low testosterone, CoQ10, carnitine, creatine promote
      1. RHABDOMYLYSIS that can cause kidney failure
      2. Promoted AUTOIMMUNE MYOPATHY
      3. HEART FAILURE
      4. LUNG IMPAIRMENT
      5. CHOLESTASIS
      6. URINARY RETENTION
      7. CONSTIPATION
      8. PERMANEANT MUSCLE DAMAGE can occur
      9. Muscle WEAKNESS, at times severe
    2. Declining exercise levels, loss of strength, and faster muscle fatigue on statins. The study in mice “suggest that statins may reduce the desire to participate in a voluntary or prescribed exercise training program.” PLOS ONE 1-2017
    3. A 19% greater risk of musculoskeletal problems e.g. strains, sprains
    4. Muscle aches are more common when combined with amlodipine or diltiazem
  36. EXERCISE:
    1. If not on statin, exercise increased cardiovascular (CV) fitness 10%, muscle mitochondrial citrate synthase 13%
    2. If on statin, CV fitness blunted to 1.5% with 4.5% DECREASE in citrate synthase

J Am Coll Cardiol 2013 Aug 20 62(8):709-14

  1. LONGEVITY (references at the end of the handout)
    1. PROMOTED AGING: prevented stem cells from performing their main functions, to reproduce and replicate other cells in the body to carry out repairs. Am J Physiol ‘15
    2. HIGH cholesterol is associated with extreme LONGEVITY
      1. LOW CHOLESTEROL is not associated with a LONGER LIFE SPAN
  2. “The widespread promotion of LDL reduction is not only unjustified, it MAY WORSEN THE HEALTH OF THE ELDERLY because LDL contributes to immune functioning, including the elimination of harmful pathogens”
  3. Cholesterol levels <200 are not associated with a longer life
    1. Most research demonstrates that higher cholesterol between 200-260 may be the healthiest
    2. In fact, research shows that cholesterol levels <150 are associated with a shorter lifespan, DEPRESSION, and CANCER
    3. LDL between 100-160 appears to be the healthiest range,
      1. But a lot depends on the type of LDL.
  4. Studies around the world consistently show: low LDL is strongly, independently associated with increased risk of cancer, CVD, and all-cause mortality.
  5. The lowest LDL (< 70 mg/dL) had a higher risk of all-cause mortality, CVD mortality, and cancer mortality
  6. Hazard ratios of all-cause and cancer mortality were particularly negatively related to total cholesterol (TC) < 200 mg/dL, especially in range < 120 mg/dL
    1. A TC ≥ 280 mg/dL correlated with mortality from CVD and cancer
  7. In people >85 years, high total cholesterol is associated with longevity owing to lower mortality from cancer and infection.
  8. Nonagenarians survival time was longer when LDL >130 mg/dL
  9. A Cochrane meta-analysis of 18 cholesterol-lowering trials (some with statins) in those with peripheral arterial disease failed to show a mortality benefit.
  10. Two different Cochrane studies on statins and mortality do not support statins as a preventive to reduce all-cause mortality
    1. One meta-analysis of 11 statin trials for high-risk primary prevention similarly failed to demonstrate a mortality benefit.
  11. Meta-analysis of 27 statin trials assessed for mortality: no benefit 
  12. Lowest risk of all-cause mortality was found at an LDL of 140 mg/dL,
    • Total Cholesterol range 50–199 mg/dL: 
      1. Each 39 mg/dL (1 mmol/L) increase associated with 23% lower mortality. TC range 200–449 mg/dL: Each 39 mg/dL increase associated with 7% higher mortality. Optimal TC ranges by age and sex:
      2. TC levels with lowest mortality were 210–249 mg/dL for most groups
      3. U-shaped associations between TC and mortality were consistent across all age-sex groups.
      4. The protective associations for TC <200 mg/dL were stronger than the harmful associations in the upper range
  13. INFECTIONS
    1. 13% increase in common infections Am J Med Sci. 2014 Mar PMID: 23426088
  14. Low cholesterol especially predisposed to infectious diseases.
  15. Skin and soft tissue infections increased British J Pharmacology 2019 https://doi.org/10.1111/bcp.14077
  16. SHINGLES risk increased 13% (17% on diabetics) on statins T Antoniou, et al. Dept Family Community Medicine, St. Michael’s Hosp, Toronto, Ontario
  17. INFLAMMATION is a bigger risk factor than cholesterol
  18. Treatment of statin-induced myopathy
    1. Ubiquinol 100-200mg am and noon
    2. L-carnitine 2-3gms 30” before breakfast & lunch
    3. Selenium methionine 200mcg daily
    4. D-ribose 5gm three times a day
    5. Tocotrienols
    6. Fish oil 3-5gm of EPA + DHA w/ balance GLA at 50% of omega-3
    7. Vitamin D high dose
    8. Gamma/delta tocopherols
    9. Creatine prevented injury, and along with vitamin D, reduces muscle aches
  19. OMEGA-3 FATTY ACIDS (e.g. fish oil) benefits may be wiped out by statins.
  20. Up to 5-fold higher IRON deficiency
  21. STATINS BLOCK KETONES 
    1. KETONES burn far cleaner – 30-40% reduction of reactive oxygen species
    2. HMG CoA reductase is same pathway to make ketones
    3. Ketone deficiency worsens brain function in brain disorders like Alzheimer’s
  22. HAIR LOSS
    1. Poorer maximal BALANCE raises concern for falls 10-27-11 Intern Med J  PMID: 22032261
  23. Flu vaccine is only half as likely to work
  24. Lowered aldosterone
  25. Postmenopausal women with new-onset type 2 diabetes had an increased risk of atherosclerotic cardiovascular disease, regardless of whether they took statins. European Journal of Epidemiology
  26. Government health-survey data spanning 10 years show that statin drug users increased calorie and fat intakes over time while nonusers did not. JAMA Int Med
  27. Increased LDL-booster PCSK9
  28. Atorvastatin increased calcium levels in rats
  29. If national guidelines were updated to a new risk equation, 40% fewer may qualify for statins to prevent heart disease (I estimate statins are used inappropriately 95% of the time; there are much, much safer approaches-JR) June 2024 JAMA Internal Medicine
[i] Kronmal RA, Cain KC, Ye Z, Omenn GS. Total serum cholesterol levels and mortality risk as a function of age. A report based on the Framingham data. Arch Intern Med 1993;153:1065-73. 10.1001/archinte.1993.00410090025004
[ii] Psaty BM, Anderson M, Kronmal RA, et al. The association between lipid levels and the risks of incident myocardial infarction, stroke, and total mortality: the Cardiovascular Health Study. J Am Geriatr Soc 2004;52:1639-47. 10.1111/j.1532- 5415.2004.52455.x
[iii] Fried LP, Kronmal RA, Newman AB, et al. Risk factors for 5-year mortality in older adults: the Cardiovascular Health Study. JAMA 1998;279:585-92. 10.1001/jama.279.8.585
[iv] Schupf N, Costa R, Luchsinger J, Tang MX, Lee JH, Mayeux R. Relationship between plasma lipids and all-cause mortality in nondemented elderly. J Am Geriatr Soc 2005;53:219-26. 10.1111/j.1532-5415.2005.53106.x
[v] Akerblom JL, Costa R, Luchsinger JA, et al. Relation of plasma lipids to all-cause mortality in Caucasian, African-American and Hispanic elders. Age Ageing 2008;37:207-13. 10.1093/ageing/afn017
[vi] Bathum L, Depont Christensen R, Engers Pedersen L, Lyngsie Pedersen P, Larsen J, Nexøe J. Association of lipoprotein levels with mortality in subjects aged 50+ without previous diabetes or cardiovascular disease: a population-based register study. Scand J Prim Health Care 2013;31:172-80. 10.3109/02813432.2013.824157
Concerns Raised in Some Statin Trials (Prior to 2005)
• Oversight by the pharmaceutical company (biased results)
• Premature trial terminations
• Under reporting of adverse events
• High numbers of patients lost to follow-up LOW CHOLESTEROL has been associated with… 

  • Preterm delivery 
  • Microcephaly 
  • Ischemic strokes 
  • Intracranial hemorrhage 
  • Atrial fibrillation 
  • Violent and impulsive behavior 
  • Depression 
  • Increased suicide attempts
    (7.33-fold in men and 15.6 fold in women) 

References: Problems with low cholesterol
1.      The effect of statins on testosterone in men and women, a systematic review and meta-analysis of randomized controlled trials. BMC Med. 2013 Feb 28;11:57. doi: 10.1186/1741-7015-11-57. Review
2.      Adverse Birth Outcome Among Mothers With Low Serum Cholesterol Pediatrics Oct 2007, 120 (4) 723-733; DOI:10.1542/peds.2006-1939
3.      Tsuji H. Low serum cholesterol level and increased ischemic stroke mortality. Arch Intern Med. 2011 Jun 27;171(12):1121-3. doi: 10.1001/archinternmed.2011.255.
4.      The Relationships between Cholesterol and Suicide: An Update. ISRN Psychiatry. 2012 Dec 23;2012:387901. doi: 10.5402/2012/387901.
5.      Low cholesterol as a risk factor for primary intracerebral hemorrhage: A case-control study. Ann Indian Acad Neurol. 2012 Jan;15(1):19-22. doi: 10.4103/0972-2327.93270.

THE STATIN MYTHOLOGY
Physicians and nurse practitioners started their careers with caring and love in their hearts. They were hijacked by the medical industrial complex which controlled the education, especially postgraduate, that they received. Medical journals that they trusted, dependent on drug company advertisement, fed them research that was compromised, and literally wrong half the time according to a long-term New England Journal of Medicine editor. 

Squeezed by insurance companies, health providers practices have been bought by hospital systems that control what they do and say – 75% are now owned. Insurance companies and hospitals once upon a time were non-profit; now they are a part of the medical industrial complex. Hospital CEOs control the providers; if providers step out of line, they are reprimanded or fired. These CEOs thrive on increasing their profits; they can also sit on drug company boards where they can receive potentially hundreds of thousands annually. A given researcher may not have financial conflicts but what if the hospital system that hires him does depend on those drug companies for precious research dollars? 

Health providers opinions about drugs undoubtedly varies; most believe research results they are fed; others may have doubts but are fearful of expressing them. And fear drives the health care system. It is only when we step outside of fear and focus on love that we can truly fulfill our potential.

“Peace I leave with you; my peace I give to you. I do not give to you as the world gives. Do not let your hearts be troubled, and do not let them be afraid.”  John 14:27

The raw data underpinning statin cholesterol drug trials is held exclusively by the Oxford-based Cholesterol Treatment Trialists Collaboration (CTTC) which receives millions in funding from statin drug companies; independent access was blocked and never released. The CTTC had signed confidentiality agreements with pharmaceutical sponsors, preventing verification. The statin story is a case study in bias and censorship.  For example, they use “run-in” periods before the trial to weed out those who couldn’t tolerate the drug, artificially lowering the adverse events detected during the trial. Often outcomes were reported in relative, not absolute, terms, exaggerating benefits that were, in reality, minuscule to the individual patient. The vast majority of statin trials are funded by the manufacturers, and almost all show benefit — except for one publicly funded study that showed the opposite. 10-23-25 The Defender, CHD

“The ignored clinical trials on statins and mortality. As a practicing internist and lipidologist, I have long been trained to believe in the cholesterol hypothesis. Statins were not just recommended; they were the gospel. Lower LDL, save lives. That mantra was repeated at every lecture, every conference, every guideline committee. But like many dogmas in medicine, the cracks are there if you dare to look. And some of the most damning cracks are found in a set of randomized trials that rarely get mentioned in the statin narrative. These are the ignored trials. Left out of the widely-cited meta-analysis by Silverman et al, they tell a story that should shake every clinician who still reflexively reaches for a statin prescription. The shocking numbers

  • In the EXCEL trial, all three pravastatin dose groups (20, 40, and 80 mg/day) showed more coronary heart deaths (CHD) than placebo. 0.50% vs 0.20% CHD mortality, a 150% relative risk increase for patients on pravastatin.
  • In DEBATE, mortality was higher on the statin: 18.1% vs 17.4% total deaths, and CHD deaths were also worse (7.5% vs 6.0%).
  • In GISSI-HF, rosuvastatin did not reduce death in patients with heart failure. In fact, total mortality was 28.75% vs 28.13%, a 2.2% relative risk increase with Crestor.
  • SEAS and CORONA fared no better: slight excess mortality on the drug side, with no life-saving signal.

“And then comes the kicker: IMPROVE-IT, the largest ignored trial, with 18,000 post-ACS patients. Adding ezetimibe to simvastatin reduced LDL a bit further but had no impact on total mortality (13.40% vs 13.56%). Placebo as the “better choice” Put bluntly: In these studies, placebo did as well, or better, than statins when it came to keeping patients alive. Not one showed a clear reduction in all-cause mortality. Some showed the opposite: more deaths on the drug. This is not the story the public, or most of our colleagues, hear. Instead, statins are sold as life-savers, when the uncomfortable truth is that in several large, well-run trials, they failed the most basic test: prolonging life. Why were we not told? Why were these trials sidelined? Why do guidelines and meta-analyses trumpet a selective version of the evidence, while ignoring the studies that do not fit the narrative? The answer, of course, is money. Billions of dollars, blockbuster drugs, careers, reputations, all at stake. It is far easier to bury inconvenient numbers than to confront them. A call to my colleagues I am not saying never prescribe a statin. But I am saying we owe our patients the truth:

  • The evidence that statins save lives is far shakier than advertised.
  • Some trials suggest the opposite, that patients may actually fare worse on drug than on placebo.
  • And yet we continue to prescribe them reflexively, as though they were vitamin pills.”

“At the very least, we must stop pretending the cholesterol hypothesis is settled science. If anything, these ignored trials should force us to re-examine whether lowering LDL is the right target at all. If you want to live It sounds heretical, but here is what the numbers show: If you want to live longer, in trial after trial, placebo was the better bet than the statin. That should give every one of us pause.” Larry Kaskel is an internist and “lipidologist in recovery” 

DONNIE YANCE, the #1 Botanical Medicine Expert in the country:

Your body naturally produces a type of cholesterol called LDL (low-density lipoprotein). While you may have heard it called “bad” cholesterol, LDL actually plays an important role in your health—it helps repair damaged tissues and build new cells throughout your body. However, LDL cholesterol can become harmful when it gets damaged by substances called “free radicals” in your bloodstream. When this happens, the damaged LDL can cause inflammation in your arteries and lead to the buildup of plaque. Over time, this plaque buildup can increase your risk of heart disease. Most studies investigating the relation between levels of LDL-C and the risk of all cause mortality have found no association[i],[ii],[iii] or an inverse association.[iv],[v],[vi] There is a inverse association that can be explained by the increased risk of all cause mortality associated with low levels of LDL-C rather than representing an actual decreased risk at high levels of LDL-C.  An interesting recent finding is that high cholesterol levels are associated with extreme longevity.[vii]

  • No study has shown an impact of statins on cardiovascular outcomes among older adults without preexisting coronary artery disease (CAD) or significant risk factors.
  • The U.S. Preventive Services Task Force guideline states that current evidence is insufficient to assess the balance of benefits and harms of statins in people older than 75 years who have no history of stroke or heart attack.
  • There is no definitive evidence that statins can prevent future CAD or death for people with CAD who are older than 80 years.

Despite the current emphasis on achieving low cholesterol levels, the fact is that low cholesterol is not associated with a longer life span. Studies show that high LDL-C is inversely associated with mortality in most people over 60 years.

If one examines the original Framingham Heart Study data (as an example) it is clear that the cholesterol levels of those who developed CHD and those who did not overlap except when the total cholesterol level exceeded 380 mg/dL or was less than 150 mg/dL.[viii]
Cholesterol levels <200 are not associated with a longer life, and most research demonstrates that higher cholesterol levels between 200 and 260 may be the healthiest range. In fact, research shows that cholesterol levels <150 are associated with a shorter lifespan, depression, and cancer. LDL cholesterol between 100 and 160 appears to be the healthiest range, but a lot depends on the type of LDL.

In a Japanese study of 347, 971 subjects, researchers tested the association between low-density lipoprotein cholesterol (LDL-C) and cardiovascular disease (CVD), cancer, and all-cause mortality in non-statin users. Five groups were defined according to baseline LDL-C concentration (<70, 70-99, 100-129, 130-159, ≥160 mg/dL). The lowest LDL-C group (LDL < 70 mg/dL) had a higher risk of all-cause mortality, CVD mortality, and cancer mortality compared to the reference group. cholesterol.[ix]

In a Danish study published in 2019, researchers set out to determine the association between levels of low-density lipoprotein cholesterol (LDL-C) and all-cause mortality, and the concentration of LDL-C associated with the lowest risk of all-cause mortality in the general population.

Among 108,243 individuals aged 20-100, 11,376 (10.5%) died during the study, at a median age of 81. The association between levels of LDL-C and the risk of all-cause mortality was U shaped, with low and high levels associated with an increased risk of all-cause mortality.

Compared with individuals with concentrations of LDL-C of  132-154 mg/dL, the multivariable adjusted hazard ratio for all-cause mortality was 1.25 for individuals with LDL-C concentrations of less than 70 mg/dL and 1.15 for LDL-C concentrations of more than 189 mg/dL.

The concentration of LDL-C associated with the lowest risk of all-cause mortality was 140 mg/dL in the overall population and in individuals not receiving lipid lowering treatment, compared with 89 mg/dL in individuals receiving lipid lowering treatment. Similar results were seen in men and women, across age groups, and for cancer and other mortality, but not for cardiovascular mortality.11

More evidence supports the link between LDL cholesterol levels and an increased risk of intracerebral hemorrhage (ICH). Results from a large, prospective longitudinal study show individuals with LDL below 70 mg/dL had a 65% increased likelihood of ICH over 9 years. Furthermore, the participants with LDL below 50 mg/dL had 169% greater risk compared with their counterparts who had levels in the 70 to 99 mg/dL range.[x]

In a U.S. study, researchers evaluated the effect of total cholesterol levels on all-cause, cardiovascular disease (CVD), and cancer mortality.

All data analyzed were obtained from the National Health and Nutrition Examination Survey 1999-2014. The sample studied comprised 14,662 men and 16,025 women, categorized as 25,429 adults aged 18-65 and 5,258 adults over 65 years old. A total of 2,570 deaths were recorded. All-cause, cardiovascular, and cancer mortality showed U-curve associations after adjusting for confounding variables in the restricted cubic spline analysis.

Hazard ratios (HRs) of all-cause and cancer mortality were particularly negatively related to TC levels in the lower range < 200 mg/dL, especially in the range < 120 mg/dL. However, the HRs of cardiovascular disease mortality in the range < 120 mg/dL were the lowest. In the upper range, a TC range of ≥ 280 mg/dL was correlated with mortality as a result of CVD and cancer.

The lowest cumulative survival rate of all-cause mortality was recorded in the lowest TC-level group, while the lowest cumulative survival rate of CVD mortality was recorded in the highest TC-level group.

The researchers concluded that too low or too high serum total cholesterol levels might correlate with adverse outcomes.[xi]
[1] Kronmal RA, Cain KC, Ye Z, Omenn GS. Total serum cholesterol levels and mortality risk as a function of age. A report based on the Framingham data. Arch Intern Med 1993;153:1065-73. 10.1001/archinte.1993.00410090025004
[1] Psaty BM, Anderson M, Kronmal RA, et al. The association between lipid levels and the risks of incident myocardial infarction, stroke, and total mortality: the Cardiovascular Health Study. J Am Geriatr Soc 2004;52:1639-47. 10.1111/j.1532- 5415.2004.52455.x
[1] Fried LP, Kronmal RA, Newman AB, et al. Risk factors for 5-year mortality in older adults: the Cardiovascular Health Study. JAMA 1998;279:585-92. 10.1001/jama.279.8.585
[1] Schupf N, Costa R, Luchsinger J, Tang MX, Lee JH, Mayeux R. Relationship between plasma lipids and all-cause mortality in nondemented elderly. J Am Geriatr Soc 2005;53:219-26. 10.1111/j.1532-5415.2005.53106.x
[1] Akerblom JL, Costa R, Luchsinger JA, et al. Relation of plasma lipids to all-cause mortality in Caucasian, African-American and Hispanic elders. Age Ageing 2008;37:207-13. 10.1093/ageing/afn017
[1] Bathum L, Depont Christensen R, Engers Pedersen L, Lyngsie Pedersen P, Larsen J, Nexøe J. Association of lipoprotein levels with mortality in subjects aged 50+ without previous diabetes or cardiovascular disease: a population-based register study. Scand J Prim Health Care 2013;31:172-80. 10.3109/02813432.2013.824157
[1] Kolovou G, Kolovou V, Vasiliadis I, Wierzbicki AS, Mikhailidis DP. Ideal lipid profile and genes for an extended life span. Curr Opin Cardiol. 2011 Jul;26(4):348-55. doi: 10.1097/HCO.0b013e32834659d4. PMID: 21478743.
[1] Kannel WB, Castelli WP, Gordon T. Cholesterol in the prediction of atherosclerotic disease. New perspectives based on the Framingham study. Ann Intern Med 1979; 90: 85-91 [PMID: 217290]
[1] Sung KC, Huh JH, Ryu S, Lee JY, Scorletti E, Byrne CD, Kim JY, Hyun DS, Ko SB. Low Levels of Low-Density Lipoprotein Cholesterol and Mortality Outcomes in Non-Statin Users. J Clin Med. 2019 Oct 1;8(10):1571. doi: 10.3390/jcm8101571. PMID: 31581520; PMCID: PMC6832139.
[1] McNamara, Damian Medscape, Low LDL Means Higher Hemorrhagic Stroke Risk, July 08, 2019, https://www.medscape.com/viewarticle/915359#vp_2; Ma C, Gurol ME, Huang Z, Lichtenstein AH, Wang X, Wang Y, Neumann S, Wu S, Gao X. Low-density lipoprotein cholesterol and risk of intracerebral hemorrhage: A prospective study. Neurology. 2019 Jul 30;93(5):e445-e457. doi: 10.1212/WNL.0000000000007853. Epub 2019 Jul 2. PMID: 31266905; PMCID: PMC6693427.
[1] He GD, Liu XC, Liu L, Yu YL, Chen CL, Huang JY, Lo K, Huang YQ, Feng YQ. A nonlinear association of total cholesterol with all-cause and cause-specific mortality. Nutr Metab (Lond). 2021 Mar 10;18(1):25. doi: 10.1186/s12986-021-00548-1. PMID: 33691735; PMCID: PMC7945313.

[i] Kronmal RA, Cain KC, Ye Z, Omenn GS. Total serum cholesterol levels and mortality risk as a function of age. A report based on the Framingham data. Arch Intern Med 1993;153:1065-73. 10.1001/archinte.1993.00410090025004
[ii] Psaty BM, Anderson M, Kronmal RA, et al. The association between lipid levels and the risks of incident myocardial infarction, stroke, and total mortality: the Cardiovascular Health Study. J Am Geriatr Soc 2004;52:1639-47. 10.1111/j.1532- 5415.2004.52455.x
[iii] Fried LP, Kronmal RA, Newman AB, et al. Risk factors for 5-year mortality in older adults: the Cardiovascular Health Study. JAMA 1998;279:585-92. 10.1001/jama.279.8.585
[iv] Schupf N, Costa R, Luchsinger J, Tang MX, Lee JH, Mayeux R. Relationship between plasma lipids and all-cause mortality in nondemented elderly. J Am Geriatr Soc 2005;53:219-26. 10.1111/j.1532-5415.2005.53106.x
[v] Akerblom JL, Costa R, Luchsinger JA, et al. Relation of plasma lipids to all-cause mortality in Caucasian, African-American and Hispanic elders. Age Ageing 2008;37:207-13. 10.1093/ageing/afn017
[vi] Bathum L, Depont Christensen R, Engers Pedersen L, Lyngsie Pedersen P, Larsen J, Nexøe J. Association of lipoprotein levels with mortality in subjects aged 50+ without previous diabetes or cardiovascular disease: a population-based register study. Scand J Prim Health Care 2013;31:172-80. 10.3109/02813432.2013.824157
[vii] Kolovou G, Kolovou V, Vasiliadis I, Wierzbicki AS, Mikhailidis DP. Ideal lipid profile and genes for an extended life span. Curr Opin Cardiol. 2011 Jul;26(4):348-55. doi: 10.1097/HCO.0b013e32834659d4. PMID: 21478743.
[viii] Kannel WB, Castelli WP, Gordon T. Cholesterol in the prediction of atherosclerotic disease. New perspectives based on the Framingham study. Ann Intern Med 1979; 90: 85-91 [PMID: 217290]
[ix] Sung KC, Huh JH, Ryu S, Lee JY, Scorletti E, Byrne CD, Kim JY, Hyun DS, Ko SB. Low Levels of Low-Density Lipoprotein Cholesterol and Mortality Outcomes in Non-Statin Users. J Clin Med. 2019 Oct 1;8(10):1571. doi: 10.3390/jcm8101571. PMID: 31581520; PMCID: PMC6832139.
[x] McNamara, Damian Medscape, Low LDL Means Higher Hemorrhagic Stroke Risk, July 08, 2019, https://www.medscape.com/viewarticle/915359#vp_2; Ma C, Gurol ME, Huang Z, Lichtenstein AH, Wang X, Wang Y, Neumann S, Wu S, Gao X. Low-density lipoprotein cholesterol and risk of intracerebral hemorrhage: A prospective study. Neurology. 2019 Jul 30;93(5):e445-e457. doi: 10.1212/WNL.0000000000007853. Epub 2019 Jul 2. PMID: 31266905; PMCID: PMC6693427.

[xi] He GD, Liu XC, Liu L, Yu YL, Chen CL, Huang JY, Lo K, Huang YQ, Feng YQ. A nonlinear association of total cholesterol with all-cause and cause-specific mortality. Nutr Metab (Lond). 2021 Mar 10;18(1):25. doi: 10.1186/s12986-021-00548-1. PMID: 33691735; PMCID: PMC7945313.

TESTOSTERONE and ERECTILE DYSFUNCTION
Both total and calculated free testosterone levels were significantly lower in subjects taking statins, when compared to the rest of the sample (hazard ratio [HR] = 0.93 and 0.26 for each decrement of total T and calculated free T, respectively). The use of statins was also associated with a reduced testis volume and a higher prevalence of hypogonadism-related symptoms and signs, as assessed by higher ANDROTEST score (HR = 1.12). J Sex Med. 2010 Apr;7(4 Pt 1):1547-56. Epub 2010 Feb 5. PMID: 20141585

International Index of Erectile Function (IIEF) scores after 6 months of statin therapy. Prior to statin therapy, the median IIEF score was 21 (range 0-25), and 57% had impairment of erectile function. After statin therapy, IIEF scores were reduced to 6.5 (range 0-25) (p<0.001), and 22% experienced new onset ED. Int J Clin Pract. 2006 Feb ;60(2):141-5. PMID: 16451283

The mean delay of onset of ED after starting statins, known for 19 cases, was 62 days (median 29 days). In 56.9% of cases, recovery occurred after withdrawal of statin, and rechallenge was positive in five cases. The association was statistically significant for all statins (adjusted ROR [aROR] = 2.4; 95% CI 1.8, 3.3), simvastatin (aROR = 2.6; 1.6, 4.1), atorvastatin (aROR = 3.4; 2.1, 5.4) and rosuvastatin (aROR = 7.1; 2.6, 19.4) [p<0.001 for all] but not for pravastatin and fluvastatin. Assessment of the association between drugs other than statins known to be at risk of ED confirmed a significant association for finasteride (Proscar) (aROR = 14.5), fibrates (aROR = 3.6), beta-adrenergic receptor antagonists (aROR = 1.5) and tricyclic antidepressants (aROR = 2.0]. Drug Saf. 2009;32(7):591-7. PMID: 19530745

More impotent men in the group of patients treated with hypolipidaemic drugs (12% vs. 5.6%). Multivariate analysis showed that erectile dysfunction was dependent on treatment with fibrate derivatives (odds ratio: 1.46) and statins (odds ratio: 1.51). We conclude that erectile dysfunction is a frequent disorder in hyperlipidaemic men. Our results suggest that this symptom could be a side-effect of hypolipidaemic drugs. J Clin Pharm Ther. 1996 Apr ;21(2):89-94. PMID: 8809645

With simvastatin 80mg/day, the pooled total testosterone level at baseline was 541 and 513 ng/dL in the placebo and simvastatin-treated groups, respectively, which declined to 536 +/- 20.5 ng/dL (-1.5%) and 474 +/- 30.4 ng/dL (-13.6%, P = .09) after treatment (mean +/- SD). The pooled free testosterone declined by 6.3% in the simvastatin group, versus a 4.9% increase in the placebo group (P = .588), while pooled bioavailable testosterone declined 10.2% in the simvastatin group and increased 1.4% in the placebo group (P = .035). Metabolism. 2000 Sep ;49(9):1234-8. PMID: 11016911

Two trials comparing simvastatin 80 mg/day with 40 mg/day among 640 men found after 48 weeks median testosterone lower by 10.3% and 7.5% respectively. Schooling CM, Au Yeung SL, Freeman G, Cowling BJ. The effect of statins on testosterone in men and women, a systematic review and meta-analysis of randomized controlled trials. BMC Medicine. 2013;11:57. doi:10.1186/1741-7015-11-57.

References: Low Testosterone From Statins

  1. Corona G, Boddi V, Balercia G, Rastrelli G, De Vita G, Sforza A, Forti G, Mannucci E, Maggi M. The effect of statin therapy on testosterone levels in subjects consulting for erectile dysfunction. J Sex Med. 2010 Apr;7(4 Pt 1):1547-56.
  2. Shin JY, Suls J, Martin R. Are cholesterol and depression inversely related? A meta-analysis of the association between two cardiac risk factors. Ann Behav Med. 2008 Aug;36(1):33-43.
  3. Giltay EJ, Enter D, Zitman FG, Penninx BW, van Pelt J, Spinhoven P, Roelofs K. Salivary testosterone: associations with depression, anxiety disorders, and antidepressant use in a large cohort study. J Psychosom Res. 2012 Mar;72(3):205-13.
  4. Roberto G, Biagi C, Montanaro N, Koci A, Moretti U, Motola D. Statin-associated gynecomastia: evidence coming from the Italian spontaneous ADR reporting database and literature. Eur J Clin Pharmacol. 2012 Jun;68(6):1007-11. Schooling CM, Au Yeung SL, Freeman G, Cowling BJ. The effect of statins on testosterone in men and women, a systematic review and meta-analysis of randomized controlled trials. BMC Med. 2013 Feb 28;11:57.

BRAIN, EYES, EARS, and NEUROPATHY
128 patients (75%) experienced cognitive ADRs determined to be probably or definitely related to statin therapy. Of 143 patients (84%) who reported stopping statin therapy, 128 (90%) reported improvement in cognitive problems, sometimes within days of statin discontinuation (median time to first-noted recovery 2.5 weeks). Of interest, in some patients, a diagnosis of dementia or Alzheimer’s disease reportedly was reversed. Nineteen patients whose symptoms improved or resolved after they discontinued statin therapy and who underwent rechallenge with a statin exhibited cognitive problems again (multiple times in some). Within this vulnerable group, a powerful relationship was observed between potency of the statin and fraction of trials with that agent resulting in cognitive ADRs (p<0.00001). Quality of life was significantly adversely affected for each of the seven assessed domains (all p<0.00000001). Pharmacotherapy. 2009 Jul ;29(7):800-11. PMID: 19558254

Psychiatric disorders represent 15% of the reactions to statins in the Norwegian database. Reactions include aggression, nervousness, depression, anxiety, sleeping disorders and impotence. Tidsskr Nor Laegeforen. 1997 Sep 20 ;117(22):3210-3. PMID: 9411859

Lovastatin did not disturb sleep initially (nights 5 through 7) but, with continued administration (nights 16 through 18), it significantly and markedly increased wake time after sleep onset and stage 1 sleep compared with baseline. By contrast, pravastatin was not associated with sleep disturbance either initially or with continued use. Neither drug caused any sleep disturbance after withdrawal. Lovastatin’s sleep disturbing effects with continued administration are attributed to its high degree of lipophilicity in contrast with the hydrophilicity of pravastatin. Clin Pharmacol Ther. 1991 Dec ;50(6):730-7. PMID: 1752118

Comparisons of the changes in performance between placebo- and lovastatin-treated subjects revealed differences for tests of attention and psychomotor speed. Am J Med. 2000 May ;108(7):538-46. PMID:

From GreenMedInfo.com – The Scope of Statin Harm: A Pattern, Not a Coincidence
The GreenMedInfo statin database documents 350+ adverse health effects across more than 30 biological pathways. These effects are not random. They cluster around a few central mechanisms, forming a coherent pattern of systemic injury. The most heavily documented categories include

Read Cracking the Cholesterol Myth: How Statins Harm The Body and Mind

 

Crestone and Beyond

Please come back and go over this exhaustive list of statin concerns for an ongoing review of the facts.

If you are taking statin drugs, or if you know others who are using these drugs, you can refer to the many links in this Journal to help reinforce your resolve to find wholesome alternatives for your blood vessel health.

Signing off from Crestone and Beyond

Associated Readings

  1. Statins: New Guidelines Aim at Prevention but Create More Patients…posted here on 4-15-26. Beware the moving goalposts by the doctor-pharma industry. “People in their 30s and 40s are now being pulled into earlier cholesterol screenings, specialized tests like lipoprotein(a) or coronary calcium scans, and, in many cases, statin regimens designed to last a lifetime.”
  2. Cracking the Myth–How Eating Eggs Helps Lower Bad Cholesterol…posted here on 4-11-26. “A study published in the American Journal of Clinical Nutrition showed that eating two eggs daily lowered LDL cholesterol, while high saturated fat diets raised it…Researchers found cholesterol from eggs did not raise LDL, but saturated fat from foods like bacon and sausage did, showing food context makes a major difference…Eggs provide cholesterol without overloading the liver, allowing it to clear LDL efficiently and preventing artery buildup that increases heart disease and stroke risk…Weekly egg intake reduced heart disease deaths by 29% and all-cause mortality by 17% in older adults, highlighting the importance of moderation for protective benefits…Choosing pastured eggs, avoiding vegetable oils, and pairing eggs with nutrient-rich whole foods further boost benefits while minimizing harmful omega-6 linoleic acid (LA) intake.”
  3. Geranylgeraniol (GG)–The Solution to Statin-Induced Muscle Pain That CoQ10 Couldn’t Solve…posted here on 3-23-26. An important article about a little known but very essential molecule that is the precursor to CoQ10 production in the liver. Here are the main points of this informative article: “Statin-associated muscle symptoms (SAMS) affect up to 29% of statin users, making it the most common reason patients discontinue these cholesterol-lowering drugs — yet the medical establishment has failed to provide an effective solution for decades…Multiple meta-analyses have shown that CoQ10 supplementation does not significantly reverse statin-induced myopathy, despite being the go-to recommendation from conventional medicine…The real culprit behind statin muscle damage is the depletion of geranylgeraniol (GG), a critical compound in the mevalonate pathway that statins block — GG is required for protein prenylation, which is essential for muscle cell survival and function…Unlike CoQ10, which is downstream in the metabolic pathway, GG is upstream and serves as the obligatory substrate for CoQ10 synthesis — supplementing with GG addresses the root cause rather than attempting to replace a downstream product…In vivo studies demonstrate that GG completely abrogates statin-induced skeletal muscle fatigue without causing adverse effects on cardiac function or blood vessel performance.” See this page of Designs for Health products that contain GG.
  4. Continuous Statin Use & Muscle Decline…posted here on 2-26-26. “A study published recently in the Journal of Cachexia, Sarcopenia and Muscle raises concerns about a possible side-effect of long-term statin drug use: a significant decline in muscle mass and function…Researchers determined that compared to those who had never taken statins, continuous statin users displayed a 25% decline in grip strength and a 73% decline in appendicular lean mass, and this was irrespective of genetic susceptibility to statin response.”
  5. Statins, Cholesterol, and the Real Cause of Heart Disease…this informative and revealing article was written by The Midwestern Doctor. Please read these main points: “Despite decades of statin use costing approximately $25 billion annually in America alone, heart disease remains the leading cause of death, suggesting the cholesterol hypothesis that drives statin prescriptions is fundamentally flawed…Studies show that lowering cholesterol with statins does not reduce heart disease, and yet these findings are ignored while statin guidelines are created by experts paid by pharmaceutical manufacturers…Malcolm Kendrick’s clotting model provides a superior explanation for heart disease: atherosclerotic plaques result from repeated damage to blood vessel linings which the body repairs with layers of clots…The medical establishment dismisses widespread reports of statin injuries as “nocebo effects,” paralleling how COVID-19 vaccine injuries were dismissed as “anxiety,” despite extensive evidence corroborating the injuries…The actual causes of heart disease — fine particulate matter from pollution and cigarettes, lead exposure, chronic stress, and endothelial damage — receive minimal research funding because effective interventions cannot be patented and sold as expensive pharmaceuticals like statins.”
  6. Saturated Fat & Cholesterol…posted here on 3-13-26. “A systematic review of randomized trials was recently published in the Annals of Internal Medicine, describing the associations between saturated fat intake and cholesterol, mortality, and major cardiovascular events. It included 17 eligible trials and over 66,000 participants, including people with and without cardiovascular disease. Overall, reducing saturated fat intake was associated with non-significant reductions in both all-cause and cardiovascular mortality, as well as non-fatal myocardial infarctions and both fatal and non-fatal strokes. Rather than using a relative risk reduction as their standard, the authors used a threshold of an absolute benefit of at least 5 for fatal events and 10 for non-fatal events per 1000 within 5 years, and concluded that reducing saturated fat intake did not meet this threshold among people with low baseline cardiovascular risk.”
  7. Huge Study Links 99% of Heart Attacks and Strokes with 4 Risk Factors…posted here on 3-14-26. “A large international study found that 99% of heart attacks, strokes, and heart failure cases were preceded by at least one measurable risk factor, meaning these events are rarely random and often develop over years…High blood pressure was present in more than 93% of people before their cardiovascular event, making it the most common, and powerful warning sign you can monitor and correct early…Most individuals had two or more risk factors before their first event, showing that elevated blood pressure, blood sugar, imbalanced cholesterol, and smoking exposure stack together to accelerate arterial damage…Total cholesterol alone does not accurately reflect your true heart risk; markers like HOMA-IR, fasting insulin, triglyceride-to-HDL ratio, and iron levels provide a clearer picture of metabolic stress driving vascular disease…Addressing root causes — improving insulin sensitivity, eliminating seed oils, building muscle, walking daily and optimizing sunlight exposure — strengthens cellular energy production, and helps protect your arteries long before crisis strikes.”