Simple 3-Step Gratitude Practice

Gratitude is more than a positive personality trait or a willy-nilly feeling. Gratitude has the power to change the lens through which we view the world, bringing us more joy, health and satisfaction. It’s easy to see the problems in life, not because we are cynical, but because we are looking for what we can improve in our lives. The downside to this is that we can skip over the miracles in our lives, taking the small gifts for granted. 

Creating a gratitude practice such as a gratitude jar, gratitude meditation or a gratitude journal is a great way to press pause on that dissatisfied inner voice constantly seeking more. 

The Definition of Gratitude

The word gratitude is derived from the Latin word gratia, which translates as grace or favor. Interestingly, the word grace is defined as “smoothness and elegance of movement” and “courteous goodwill,” which speaks of bringing flow and harmony into your life. 

Another phrase for gratia in Latin is “gratus animus.” Gratus means grateful, agreeable, pleasing, acceptable and welcome. Animus means heart, mind, affections, purpose and feeling. Much of human life is about kindness and compassion (giving and receiving), which makes a gratitude practice so transformative. 

Recognizing and affirming benevolence has a vitalizing effect on the mind, body and spirit. That might be why gratitude is at the core of every major spiritual tradition. The roots of a gratitude practice must be in selflessly rejoicing in the other and seeking opportunities for giving, rather than using it as a narcissistic self-improvement technique. 

A practice of gratitude will help you to live a wonderful life, and is the opposite of being entitled. Rather, a practice of gratitude is rejoicing in the gifts and wonders of life. Gratitude has been established as a universal human attribute suggesting that it is at the core of our very being. 

The Healing Power of Gratitude

Gratitude has amazing powers of improving mental health and has proven in clinical trials to have long lasting healing properties. It promotes feelings of love and tenderness toward other people and life experiences. A deep practice of gratitude also has the power of alleviating trauma, due to its other-directed understanding. 

Gratitude is used in a clinical setting with Accelerated Experiential Dynamic Therapy (ADEPT). ADEPT was designed by American psychologist Diana Fosha. The premise is that we are all capable of self-healing and transformation in the right environment. ADEPT is designed to create a deep emotional connection with both yourself and other people. 

“Be content with what you have; rejoice in the way things are. When you realize there is nothing lacking, the whole world belongs to you.”  —Lao Tzu

In the paper Gratitude as a Psychotherapeutic Intervention published by Yale Center for Emotional Intelligence and the University of California, the writers astutely wrote: “Losing some aspects of one’s life may lead the person to increase the value they see in other aspects of life.” 

Gratitude Breeds Connection

We all know that it’s nice to get gifts, but the feeling of joy from material objects is fleeting. Taking the time to be truly thankful for all of the blessings in your life will open doors. Our life depends on the existence of everything in the universe, from the sun and moon to the oceans and trees. And each person can play a special role in our lives. Taking the time to write a thank you note to spread the love has also been shown to benefit those with mental health challenges. 

“With this attitude, people recognize that they are connected to each other in a mysterious and miraculous way that is not fully determined by physical forces, but is part of a wider, or transcendent context.”  -Streng (1989) 

Gratitude can be seen as the elemental life force that powers compassion. We are all intricately connected and as such a practice of gratitude gives thanks to the interdependence, interpenetration, and mutuality of living. 

Gratitude isn’t merely positive thinking; it is a deep appreciation for life. Contrast can also be viewed through the eyes of gratitude. Pain and affliction can be released when they are contrasted with more positive aspects of the now. No matter how small, there is always something to be grateful for. 

What does a Gratitude Practice Look Like?

In the first instance you can simply pay attention to what is going well in your life. Taking time to shift your focus from the negative to the positive. A gratitude practice should include the understanding that even painful situations are teachers. The simple act of redirecting our focus can take us from a place of victimhood to appreciation, altering our view of the world. 

Simple 3-Step Gratitude Practice

• Step 1 – Attention – become aware of the blessings in your life that you may have taken for granted. 
• Step 2 – Tune into the many reasons for gratitude that exist in our lives. 
• Step 3 – Write it down – Writing is scientifically proven to be more powerful than simply thinking thoughts of gratitude. You can choose to write down one thought a day and place it in a gratitude jar. Or you may like to keep a special gratitude journal and write down 5-10 blessings every day. 

If you choose to use a gratitude jar, you can amplify the benefits by sharing the experience with your family. Sharing a gratitude jar will encourage family members to have a grateful outlook on life. Counteracting feelings of entitlement, envy, and resentment, which are negative feelings that push people away from us. A  gratitude jar encourages each member of the family to practice thinking in a positive way that will bring joy, prosperity and connection into your home. 

“Always be rejoicing. Give thanks for everything.”  -1 Thessalonians 5:16, 18.

In Conclusion

Gratitude intervention remains an untapped therapeutic resource that can be used by anyone, especially those working in healthcare settings. Changing the perspective of a patient from one of despair to gratitude could catalyze their healing process. Adding gratitude techniques is an easy way to boost your self esteem and that of those around you. 

Topical Progesterone, Not Synthetic Progestins or Oral Progesterone, Should Be Considered as a Companion for Estradiol Replacement Therapy

Dr. David Zava Friday, January 17, 2020

In 2002 several large-scale clinical studies were published on the risks of breast cancer in postmenopausal women using conventional FDA-approved hormone therapy. These were the Women’s Health Initiative (WHI) and Million Women’s studies of women using FDA-approved estrogens and progestogens in the United States and Great Britain, respectively [1,2]. Both studies came to the same conclusion – that estrogen therapy, mostly in the form of oral conjugated equine estrogens, by itself did not significantly increase the risk of breast cancer and, to the surprise of many, was associated with a lower risk. However, when estrogen was combined with a synthetic progestin to prevent uterine cancer, the breast cancer risk increased 1.5 to 2-fold. Virtually all forms, of which there are many, of synthetic progestins increased risk to about the same extent. Smaller studies suggested that FDA-approved oral progesterone, which was not as widely used, did not increase risk in combination with estrogen therapy. These results led to widescale panic among postmenopausal women using conventional estrogen and progestogen (both synthetic progestins and natural progesterone) therapies and a precipitous drop in prescriptions for these forms of HRT [1]. Many women stopped cold turkey all forms of hormone replacement therapy (HRT), which significantly diminished their quality of life. Adverse estrogen deficiency symptoms that were effectively suppressed with estrogen therapy (e.g., hot flashes and night sweats, sleep disturbances, memory issues, incontinence, vaginal dryness, depression, weight gain, etc.) resurfaced with a vengeance in many women, as did risk for diseases of advanced aging (e.g., bone loss and osteoporosis, cardiovascular disease, stroke, diabetes, senile dementia, Alzheimer’s disease). Women were left frightened between “damned if you do and damned if you don’t,” and a large majority chose not to continue HRT. Many health care providers refused to prescribe hormone therapy until more information about risks were made available through clinical trials.

Natural Progesterone Reduces Breast Cancer Risk

It was clear to me from the research literature and smaller clinical studies that the natural hormone progesterone, when delivered topically at a physiological dose (25 mg) protects normal breast tissue from the growth promoting actions of estrogens.

When these and other studies emerged in 2002 John Lee, MD, and I along with Virginia Hopkins had just published our book entitled, “What Your Doctor May Not Tell You About Breast Cancer: How Hormone Balance Can Help Save Your Life” [3]. The short of the book is that if your hormones are out of balance and you are suffering from symptoms and conditions of advancing age, meaning the transition into menopause and beyond, then you should replenish your hormones back to physiological levels with the same hormones that your body made when you were healthy early middle age. This meant if you were to use estrogen replacement therapy (ERT) you would replace with estradiol and/or estriol, not a synthetic estrogen like ethinyl estradiol (synthetic estrogen found in birth control pills) or a conjugated horse estrogen (Premarin). And if you were taking a progestogen to help balance the estrogen and protect against its proliferative effects, use bioidentical progesterone, not a synthetic progestin like medroxyprogesterone acetate (Provera) or other synthetic “fake” progesterone. We already knew from earlier studies published several years before WHI that the synthetic progestins were increasing the incidence of breast cancer [3, Chapter 11]. As a research scientist at that time, who had spent 20+ years researching and publishing on the role of estrogen and progestogen binding to their receptors and regulating breast cell proliferation and differentiation, it was clear to me from the research literature and smaller clinical studies that the natural hormone progesterone, when delivered topically at a physiological dose (25 mg) protects normal breast tissue from the growth promoting actions of estrogens [4]. In the breast cancer book [3] we delved into a lot more of what the scientific literature says causes breast cancer and what can be done to help prevent it, like avoid bad foods and environmental chemicals, make sure you’re eating good nutritious foods with plenty of colored vegetables, exercise in moderation, get adequate sleep in the dark, reduce stress as much as possible to lower cortisol-induced estrogen, and take nutritional supplements that bolster the army of antioxidants that protect against environmental toxins that convert good estrogens to bad ones [5,6]. And if your hormones are out of balance, based on testing their levels in body fluids that represent the bioavailable fraction that enters cells, use physiological amounts of bioidentical hormones to adjust them to levels when you were younger and healthy. What has been crystal clear is that bioidentical hormone therapy, if used correctly and in physiological amounts, will significantly reduce risk but is no guarantee you will never develop breast cancer.

Synthetic Progestins Raise Breast Cancer Risk

Fast forward about 20 years to present; several more recent meta-analyses of the risk of breast cancer with FDA-approved, or equivalent for non-US countries, estrogen and progestogen therapies, shed some new light on risk of HRT for breast cancer. These studies (US, British) mostly just reiterated what we already knew: that estrogen therapy only increases breast cancer risk slightly, but significantly when combined with synthetic progestins [1]. The meta-analysis of prospective studies of slightly over 100,000 women using estrogen alone or estrogen combined with progestogens (mostly synthetic), but also oral progesterone [1], revealed that estrogen therapy alone was only associated with a slight increase in risk, but when combined with a synthetic progestin the risk was approximately doubled after 5 years and doubled again at 10 years of use. No question, synthetic progestins were bad for the breasts and should not be used, especially by women who want to reap the many benefits of hormone therapies their entire lives, who should avoid synthetic progestins. Most surprising was that this study also reported that FDA-approved oral bioidentical progesterone, combined with estrogen, carried the same approximately 2-fold higher risk at 5-10 years, but strangely had no increased risk less or greater than that [1]. No data were available for topical progesterone combined with estrogens, perhaps because very few, if any, clinical studies have been carried out in the US or Great Britain and surrounding European countries using natural progesterone delivered topically. 

Topical versus Oral Progesterone

Oral progesterone, while it protects the endometrial lining, may not raise progesterone to a level high enough to counter the growth-promoting actions of estrogens in the breast tissue.

Despite research and small clinical studies showing that natural progesterone delivered topically directly to the breasts of humans [4] and primates protects against estrogen-stimulated cell proliferation of normal mammary epithelial cells, a risk factor for breast cancer, surprisingly no large prospective randomized clinical studies have been carried out to investigate if topical progesterone therapy is associated with reduced risk for developing breast cancer. The reason for this is not based on science, but economics. Progesterone cannot be patented; however, progesterone combined with a special delivery system can be, as seen with several forms of FDA-approved oral progesterone (Prometrium and Bijuva). Oral progesterone, however, while it protects the endometrial lining, may not raise progesterone to a level high enough to counter the growth-promoting actions of estrogens in the breast tissue [7].

Factors Influencing Estrogen Metabolism to Mitigate Risk

What is clear is that anything that reduces excessive estrogen burden, be it progesterone, natural or synthetic aromatase inhibitors, diet with more fiber and phytochemicals with colored vegetables, exercise, stress reduction, better sleep habits, etc., translates to lower breast cancer risk. That is what progesterone does. It lowers cell proliferation by down-regulating estrogen receptors (ER), preventing further estrogen-mediated stimulation of cell proliferation and redirects differentiation through progesterone interaction with estrogen-regulated cellular progesterone receptors (PR). Progesterone, via its activation of 17β-hydroxysteroid dehydrogenase type 2 (see diagram below), also increases the conversion of estradiol, a potent estrogen with high affinity for cellular ERs, to estrone, a weak inert estrogen [3]. Progesterone also enhances synthesis of sulfotransferase, an enzyme that then sulfates estrone to estrone sulfate, which is unable to enter cells and serves as a circulating estrogen precursor that must be converted back through two enzymatic steps, sulfatase and 17β-hydroxysteroid dehydrogenase type 1, to estradiol.

Diagram depicts the progesterone-regulated metabolism of E2 to E1 and then to E1-SO4, and then Cyp1A1 and Cyp1B1 conversion, respectively, to 2- and 4-hydroxy estrogens and their further oxidation to 2- and 4-quinones. For details see reference [5].

Progesterone’s Effects on Estrogen-Stimulated Cell Proliferation

What is poorly understood in the scientific/clinical community is that progesterone has dual actions in its effects on estrogen-stimulated cell proliferation. At the lower luteal levels (about 1-10 ng/mL) progesterone synergizes with estrogen to promote cell proliferation with little differentiation. If insufficient progesterone is produced in the presence of high estradiol, as often occurs at perimenopause with compromised luteal function, proliferation may be higher than with estradiol alone [7]. However, at higher luteal levels (10-30 ng/mL) progesterone counters the growth-promoting actions of estrogen by down-regulating ER, and through induction of cellular PR redirects the cellular machinery to drive quiescence and differentiation, causing proliferation to come to a halt. If inadequate progesterone is present, as often happens at the transition to menopause (perimenopause) when the corpus luteum fails to produce adequate progesterone but abundant estrogen (low progesterone/estradiol ratio), then the combination of higher physiological estrogen and lower luteal progesterone (in range, but low-normal) will often result in persistent proliferation and the clinical manifestation of fibrocystic and painful breasts. Excessive proliferation in the absence of progesterone increases risk for gene mutations that have the potential to lead to increased breast cancer risk. 

Risks Greatest During the Menopausal Transition

Retrospective clinical studies have shown that the higher the luteal progesterone level 5 years prior to breast cancer diagnosis, the lower the risk of developing breast cancer.

As shown in the diagram above, estrogens in excess, in the absence of progesterone and with exposure to environmental toxins, induce the cytochrome enzyme Cyp1B1 that converts beneficial estradiol to potentially toxic and mutagenic 4-catechol estradiol [5,6]. During this perimenopausal transition is when the rate of increase of breast cancer is greatest. Retrospective clinical studies have shown that the higher the luteal progesterone level 5 years prior to breast cancer diagnosis, the lower the risk of developing breast cancer [8], so it is important to keep progesterone balanced with estradiol, especially during the menopause transition when estrogen metabolite damage is most likely to occur, as shown in a recent study on estrogen metabolite formation and breast cancer risk [6].

Topical Progesterone Achieves Optimal Tissue Levels

As mentioned, oral progesterone, because it is mostly degraded (90-95%) in the GI tract and liver to metabolites with no capacity to bind and activate PR, may not reach sustained luteal levels to counter the growth-promoting actions of estrogens. Based on saliva, capillary blood, and tissue levels of progesterone, only topically applied progesterone [9] can achieve capillary blood and tissue levels of progesterone high enough to counter the proliferative actions of estrogens. While small clinical studies have shown that topical progesterone used at physiological dosing (25-50 mg) effectively reduces estrogen-induced proliferation of the mammary epithelium in humans [4], this form of therapy has not been tested in a large scale prospective case-control randomized study as with FDA-approved conjugated equine estrogens in combination with synthetic progestins [1,2].

What might we learn from what we know about the dual actions of progesterone as it relates to bioidentical estrogen and progesterone therapies for menopausal women and their risk for breast cancer? If we let mother nature be our guide, then we should strive to keep estrogen within the physiological ranges seen throughout a full monthly cycle (about 50-150 pg/mL in serum or about 2% of that seen in saliva, 1-3 pg/mL). For at least half of the month serum or capillary blood (Dried Blood Spot, DBS) progesterone should be about 10-30 ng/mL and saliva 200-600 pg/mL. This results in a progesterone/estradiol ratio of about 100-300, which is consistent with the ratio seen at the peak of the luteal phase and shown to be protective of the breasts exposed to estradiol [4]. Excessive estradiol or too little progesterone will result eventually in estrogen dominance and symptoms of estrogen excess (e.g., weight gain in the hips and thighs, fibrocystic and painful breasts, mood swings, etc.) Those are warning signs. High levels of 4-catechol estrogens ratchet that up to extreme warning [5] as we have found that 4-catechol estrogens are much higher in women harboring breast cancers than healthy women [6]. 

Many providers believe that topical progesterone is ineffective because it doesn’t raise serum levels. To the contrary, we [9] and others [4,10] have shown that physiological dosing with topically delivered progesterone raises the progesterone to physiological levels in tissues of the body such as the salivary gland, and capillary beds of the finger tips. High dose progesterone (> 50 mg), in an attempt to achieve physiological concentrations in serum never does this, regardless of the topical progesterone dose [9]. What may seem paradoxical based on serum levels is that excessive progesterone and too little estrogen will eventually keep ER persistently down-regulated and may precipitate symptoms of estrogen deficiency with weight gain, vasomotor symptoms, excessive sleepiness, etc. Keep in mind that estradiol and progesterone are produced in a rhythmic pattern each month. Estradiol rises slowly throughout the first half of the cycle and peaks about midway with ovulation. This stimulates growth and proliferation of the uterus and breasts. Progesterone will not work if there is no cellular PR, which requires adequate ER. Excessive progesterone down-regulates ER, stopping the cycle.

In summary, maintaining estradiol levels in balance with natural progesterone is necessary to achieve optimal clinical benefits of these hormones. It is the opinion of this author that these goals for optimal progesterone therapy as a breast cancer preventive can best be achieved with topical progesterone, and not oral progesterone, or a synthetic progestin. However, clinical studies with topical progesterone are needed to confirm this hypothesis.

While you go through the stages of menopause, it is important to get your hormone levels checked to ensure that you are within physiological levels. If you are going into, in the middle of, or at the end of your menopause journey, ZRT’s saliva and blood spot testing can give you the information necessary to get your hormones balanced and get you back to optimal health.

This article was first published in the American Academy of Anti-Aging Medicine (A4M) Winter 2019 Issue.

Related Resources

• Blog: Genetic Sequence Variations and Breast Cancer Risk
• Blog: Topical Delivery of Sex Steroid Hormones and Distribution in Different Body Fluids
• Blog: New Research Shows Natural Progesterone Can Help Treat Breast Cancer Part 1 and Part 2

References

[1] Collaborative Group on Hormonal Factors in Breast Cancer. Type and timing of menopausal hormone therapy and breast cancer risk: individual participant meta-analysis of the worldwide epidemiological evidence. Lancet. 2019;394:1159-68.

[2] Manson JE, WHI Investigators, et al. Menopausal Estrogen-Alone Therapy and Health Outcomes in Women With and Without Bilateral Oophorectomy: A Randomized Trial. Ann Intern Med. 2019;171:406-414.

[3] Lee JR, Zava D, Hopkins V. What your doctor may not tell you about breast cancer – how hormone balance can help save your life. Warner Books, 2002.

[4] Chang KJ, et al. Influences of percutaneous administration of estradiol and progesterone on human breast epithelial cell cycle in vivo. Fertil Steril. 1995;63:785-91.

[5] Cavalieri EL, et al. Molecular origin of cancer: catechol estrogen-3,4-quinones as endogenous tumor initiators. Proc Natl Acad Sci USA. 1997;94:10937-42.

[6] Miao S, et al. 4-Hydroxy estrogen metabolite, causing genomic instability by attenuating the function of spindle-assembly checkpoint, can serve as a biomarker for breast cancer. Am J Transl Res. 2019;11:4992-5007.

[7] Sitruk-Ware LR, et al. Inadequate corpus luteum function in women with benign breast diseases. J Clin Endocrinol Metab. 1977;44:771-4.

[8] Micheli A, et al. Endogenous sex hormones and subsequent breast cancer in premenopausal women. Int J Cancer. 2004;112:312-8.

[9] Du JY et.al. Percutaneous progesterone delivery via cream or gel application in postmenopausal women: a randomized cross-over study of progesterone levels in serum, whole blood, saliva, and capillary blood. Menopause 2013;20:1169-75.

[10] Leonetti HB, et al. Topical progesterone cream has an antiproliferative effect on estrogen-stimulated endometrium. Fertil Steril. 2003;79:221-2.

• 1 drop = approximately 60 mg
• 1 ml = 1/5 teaspoon
• 1ml = approximately 16 drops
• 1 ml = fills one 00 capsule
• 5 ml = 1 teaspoon
• 5 ml = approximately 80 drops
• 15 ml = 1 tablespoon
• 15 ml = 1/2 fluid ounce
• 240 ml = 1 cup (depends on product)
• 30 ml = 1 fluid ounce
• 28 grams = 1 ounce
• 16 ounces = 32 tablespoons

Hormonal Posts Compilation

Hormonal Information

Hormone Excesses & Deficiencies

Power of Progesterone

Progestin vs. Progesterone: A Case of Mistaken Identity

Endometriosis: A Disorder of Estrogen Dominance

Menstrual  Cramps

Compilation of Older Hormonal Posts

Hormonal Information

Power of Progesterone

Hormone Excesses & Deficiencies

Endometriosis: A Disorder of Estrogen Dominance

Progestin vs. Progesterone: A Case of Mistaken Identity

Menstrual  Cramps

Statins Shown to Extend Life by Mere Days

https://youtu.be/ooe4w9Jw2U4?list=PL7YKya_R1ROv4NteXvsG4PixMsLxcFVK1

Google Dr.Malcom Kendrick–he offers an enormous format of information on Statin Drugs

Story at-a-glance

• A 2015 systematic review of statin trials found that in primary prevention trials, the median postponement of death was just 3.2 days. In secondary prevention trials, death was postponed 4.1 days
• A 2018 review presents substantial evidence that total cholesterol and LDL cholesterol levels are not an indication of heart disease risk, and that statin treatment is of “doubtful benefit” as a form of primary prevention for this reason
• Tactics used in statin studies to exaggerate benefits include excluding unsuccessful trials, cherry-picking data, ignoring the most important outcome — an increase in life expectancy — and using a statistical tool called relative risk reduction to amplify trivial effects
• If you look at absolute risk, statin drugs benefit just 1% of the treated participants. Out of 100 people treated with statins for five years, one person will have one less heart attack
• Statin trials minimize health risks by using a run-in period. Participants are given the drug for a few weeks, after which those who suffer adverse effects are simply excluded, thereby lowering the perceived frequency and severity of side effects

Researchers have repeatedly failed to find evidence that high cholesterol is a risk factor for cardiovascular disease. In fact, there’s plenty of evidence suggesting that higher cholesterol may actually be healthier than lower levels.

As I’ve discussed in many previous articles, three (to some degree interrelated) factors that have a far greater influence on your cardiovascular disease (CVD) risk are:

• Insulin resistance¹
• Chronic inflammation²
• High iron³

Elevated iron levels will significantly contribute to inflammation, but even if your iron is normal, chronic inflammation can be caused by a wide range of factors, starting with your diet. Your diet is also the key factor at play when it comes to your insulin level, and can worsen the effects of iron overload.

Unfortunately, these primary contributors are rarely the focus of CVD prevention and treatment in conventional medicine. Instead, statins (cholesterol lowering drugs) are the go-to first line of defense, and this despite the many studies showing cholesterol isn’t a part of the problem.

Eye-Opening Finding: Statins Extend Life by About Three Days

A systematic review⁴ published in 2015 that deserves far more attention than it has received assessed the ability of statins to postpone death and improve mortality rates. Eleven statin trials with a follow-up between two and 6.1 years were included in the review.

In primary prevention trials (meaning studies in which statins were used as a primary prevention for CVD), death was postponed between a negative five days (meaning they died five days sooner than the control group) and 19 days.

In secondary prevention trials, death was postponed between a negative 10 days and 27 days. The median postponement of death in primary prevention trials was 3.2 days, and in secondary prevention trials 4.1 days.

This is a truly astounding finding, considering people take stains for years, if not decades, and the fact that these drugs are associated with a wide range of serious side effects that can decimate quality of life.

British MP Calls for Parliamentary Inquiry Into Statins

The good news is, more and more scientists are now starting to see this truth. A March 9, 2019, article⁵ in European Scientist reported:

“Earlier this week, the Chair of the British Parliament Science and Technology Committee, Sir Norman Lamb MP made calls for a full investigation into cholesterol lowering statin drugs.

It was instigated after a letter was written to him signed by a number of eminent international doctors including the editor of the BMJ, the Past President of the Royal College of Physicians and the Director of the Centre of Evidence Based Medicine in Brazil … calling for a full parliamentary inquiry into the controversial medication.”

In the article, the lead author of the letter, cardiologist Aseem Malhotra, discusses the dangers of statins, and how the flawed cholesterol hypothesis and the corresponding low-fat myth are pushing patients’ health in the wrong direction. He writes, in part:⁶

“It is not just financial interests that bias research findings but also intellectual hubris in medicine too. It was the father of the evidence based medicine movement the late Professor David Sackett who said ‘Fifty percent of what you learn in medical school will turn out to be either outdated or dead wrong within five years of your graduation, the trouble is no one can tell you which half so you have to learn to learn on your own.’

In the past 30 years, there have now been 44 randomized controlled trials that reveal no cardiovascular mortality benefit from diet or various drug trials from lowering cholesterol.

Most conspicuous was the recent ACCELERATE trial with over 12,000 patients at high risk of heart disease that revealed no reductions in heart attack, stroke or death despite a 37% reduction in LDL-cholesterol.

But how many doctors actually keep up with the latest evidence? Many will defend the cholesterol lowering dogma with their more inquisitive patients by saying they’re just following guidelines, unaware that the guidelines themselves are based upon biased research often written by scientists with strong personal or institutional financial ties to the industry.”

Scientific Review Declares Statin Claims Are Overblow

Another newsworthy review⁷ that ties into Malhotra’s arguments against statins was published in the Expert Review of Clinical Pharmacology in September 2018. It identified significant flaws in three recent studies “published by statin advocates” attempting “to validate the current dogma.”

The paper presents substantial evidence that total cholesterol and low-density lipoprotein (LDL) cholesterol levels are not an indication of heart disease risk, and that statin treatment is of “doubtful benefit” as a form of primary prevention for this reason. The paper also details the tactics used in statin studies to exaggerate the benefits. Among them:

• Excluding unsuccessful trials where statins either had no or negative impact on CVD risk or mortality

• Using “evidence” that isn’t a true exposure-response

• Cherry-picking data that supports the conclusion of benefit

• Ignoring the most important outcome — an increase in life expectancy

• Using a statistical tool called relative risk reduction to amplify trivial effects — This was also addressed more directly in a 2015 report^8,9 titled “How Statistical Deception Created the Appearance That Statins Are Safe and Effective in Primary and Secondary Prevention of Cardiovascular Disease.”

Here, the authors point out that if you look at absolute risk, statin drugs benefit just “1% of the treated participants.”¹⁰ This means that out of 100 people treated with the drugs for five years, one person will have one less heart attack.

According to the authors of the 2018 review:¹¹

“For some years, many researchers have questioned the results from statin trials because they have been denied access to the primary data. In 2004–2005, health authorities in Europe and the United States introduced New Clinical Trial Regulations, which specified that all trial data had to be made public. Since 2005, claims of benefit from statin trials have virtually disappeared.”

How Statin Studies Minimize Appearance of Side Effects

The Expert Review of Clinical Pharmacology paper also points out that statin trials minimize health risks by using a run-in period. Essentially, the participants are given the drug for a few weeks, after which those who suffer adverse effects are simply excluded.¹² Needless to say, this automatically lowers the number of perceived side effects.

In reality, serious side effects may affect anywhere from 20% to 50% of statin users.¹³ What’s more, muscle damage is likely far more common a side effect than most statin studies claim.

The authors cite one study in which myopathy occurred in just 0.01% of treated individuals. However, myopathy was defined as having a creatine kinase level “more than 10 times higher than normal,” the authors note.¹⁴

Meanwhile, other research that looked at muscle biopsies found patients with normal creatine kinase levels, who complained of muscular symptoms, indeed had microscopic signs of myopathy. “When patients stopped treatment, their symptoms disappeared, and repeated biopsies showed resolution of the pathological changes,” the authors note, adding that:¹⁵

“To reject the frequent occurrence of muscular problems with the argument that muscle symptoms are nocebo effects is also invalid. In a study of 22 statin-treated professional athletes, the authors reported that 17 (77%) of the athletes terminated treatment because of muscular symptoms, which disappeared a few days or weeks after drug withdrawal.

The explanation for statin-induced adverse muscle effects is probably that statin treatment not only blocks the production of cholesterol but also blocks the production of several other important molecules, for instance, coenzyme Q10, which is indispensable for energy production.

As most energy is produced in the muscle cells, including those of the heart, the extensive use of statin treatment may explain the epidemics of heart failure that have been observed in many countries.”

Another study¹⁶ published in 2011 supports these statements, concluding that statin treatment lasting longer than two years causes “definite damage to peripheral nerves.”

A study¹⁷ published in the August 2019 issue of JACC: Basic to Translational Science presents a new mechanism of statin-induced myopathy. In short, the data suggest statin treatment causes calcium to leak out of your muscle cells.

As explained by Science Daily,¹⁸ “Under normal conditions, coordinated releases of calcium from these stores make the muscles contract. Unregulated calcium leaks may cause damage to muscle cells, potentially leading to muscle pain and weakness.”

Statin Use Is Associated With a Wide Variety of Problems

In their Expert Review of Clinical Pharmacology paper, the authors also highlight research showing statin use is associated with a number of significant health complications beside muscle problems:¹⁹

“… [C]ase–control and cross-sectional studies have shown that statin use is observed significantly more often among patients with cataracts, hearing loss, suicidal ideation, peripheral neuropathy, depression, Parkinson’s disease, interstitial cystitis, herpes zoster, impotency, cognitive impairments, and diabetes.

In some of these studies, the side effects disappeared with discontinuation of the statins and worsened with rechallenge. As cholesterol is a vital substance for the renewal of all cells, and since statins also block the production of other molecules necessary for normal cell function, it is not surprising that statin treatment may result in side effects from many different organs.”

Even More Reasons to Avoid Statin Drugs

The scientific fact is, aside from being a “waste of time” and not doing anything to reduce mortality, statins also come with a long list of potential side effects and clinical challenges. Importantly, statins:

1. Deplete your body of CoQ10 — Statins block HMG coenzyme A reductase in your liver, which is how they reduce cholesterol. But this is also the same enzyme that makes CoQ10, which is an essential mitochondrial nutrient that facilitates ATP production.

2. Inhibit the synthesis of vitamin K2, a vitamin that protects your arteries from calcification.

3. Because of 2 and 3, statins increase your risk for other serious diseases. Aside from the conditions mentioned above, they may also raise your risk for:

a. Cancer — Research²⁰ has shown that long-term statin use (10 years or longer) more than doubles women’s risk of two major types of breast cancer: invasive ductal carcinoma and invasive lobular carcinoma.

b. Diabetes — Statins have been shown to increase your risk of diabetes via a number of different mechanisms, two of which include increasing your insulin resistance, and raising your blood sugar. According to one recent study,²¹ statins double your risk of Type 2 diabetes, and triple the risk when taken for more than two years.

c. Cognitive dysfunction, neurological damage²² and neurodegenerative diseases, including vascular dementia, Alzheimer’s disease and Parkinson’s disease.²³

d. Decreased heart function.²⁴

e. Impaired fertility — Importantly, statins are a Category X medication,²⁵ meaning they cause serious birth defects,²⁶ so they should never be used by a pregnant woman or women planning a pregnancy.

Statins Do Not Benefit Patients With Respiratory Disease

Aside from lowering cholesterol, statins appear to have an ameliorating effect on inflammation. For this reason, statins are at times used in the treatment of pulmonary conditions such as chronic obstructive pulmonary disease (COPD). This may be because statins are a Nrf2 activator²⁷ and decrease oxidative stress and secondary inflammation.

However, while some observational studies have shown a potential benefit, a July 2019 systematic review²⁸ by the Cochrane Database of Systematic Reviews failed to find any significant benefit for this patient group. The review had three primary objectives:

a. To determine whether statins reduce mortality rates in COPD

b. To determine whether statins reduce exacerbation frequency, improve quality of life, or improve lung function in COPD

c. To determine whether statins are associated with adverse effects

The review included eight placebo-controlled studies involving 1,323 participants with COPD, with a mean age of 61.4 to 72 years. According to the authors:²⁹

“We found no statistically significant difference between statins and placebo in our primary outcome of number of exacerbations per person‐year, including number of exacerbations requiring hospitalization per person‐year …

Our primary outcomes of all‐cause mortality and COPD‐specific mortality showed no significant difference between statins and placebo, with wide confidence intervals suggesting uncertainty about the precision of the results … Results show no clear difference in quality of life, which was reported in three trials …

A small number of trials providing low‐ or moderate‐quality evidence were suitable for inclusion in this review. They showed that use of statins resulted in a reduction in CRP and IL‐6, but that this did not translate into clear clinical benefit for people with COPD.” 

Beware: Next-Gen Cholesterol Drugs Likely Just as Harmful

While some of the dangers of statins are becoming more widely recognized, the dangers of cholesterol-lowering drugs in general is still being swept under the rug as newer drugs are being released.

One next-gen class of cholesterol-lowering drugs is the proprotein convertase substilisin/kexin type 9 (PSCK9) category, also known as PCSK9 Inhibitors.³⁰ Just as there are many different drugs within the statin category, there are many in the PSCK9 category. Repatha is one of them.

PCSK9 is a protein that works with LDL receptors that regulate LDL in your liver and release LDL cholesterol into your blood. The inhibitors work by blocking that protein, thus lowering the LDL in circulation.

While these drugs are being touted as the answer for those who cannot tolerate some of the side effects of statins, such as severe muscle pain, there’s already evidence suggesting PCSK9 inhibitors can produce neurocognitive effects, with some patients experiencing confusion and attention deficits.^31,32,33,34

At the end of the day, if you’re concerned about your heart health, you’d be wise to implement lifestyle changes known to support a healthy heart and help prevent CVD from developing in the first place. You can learn more about your risk factors, recommended tests and drug-free prevention methods in the following articles: “Cholesterol Does Not Cause Heart Disease,” “How to Increase Your Health Span,” and “Why Your Doctor Is Wrong About Cholesterol.”