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
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
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
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
“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.
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.
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
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
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” .
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 . In the breast cancer book 
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 .
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 ,
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 .
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 
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 .
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
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 .
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 .
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
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 ,
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 .
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
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 ,
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 . 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  as we have found that 4-catechol estrogens are much
higher in women harboring breast cancers than healthy women .
Many providers believe that topical progesterone is ineffective because it doesn’t raise serum levels. To the contrary, we  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 .
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
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.
Women have it so easy don’t they? Forget high heels and more expensive dry cleaning bills. Those are mild compared to menarche, menopause, and about forty years of menstruation in between. Under the best of circumstances, the hormonal fluctuations that accompany these events can make life “interesting” for the women experiencing them as well as for the men who are close to them. (Not to mention their kids and coworkers!) But throw in the curveballs of modern life—poor diet, inadequate sleep, relentless psychological stress, and an environment rife with inescapable estrogenic compounds in manmade goods—and the effects on a woman’s hormones make towering amusement park roller coasters look like the kiddie teacup ride.
The modern functional medicine practitioner is likely to encounter female patients presenting with issues resulting from excess estrogen, inadequate progesterone, or both. Such imbalances may occur in women of reproductive age as well as post-menopausal women, and they can have a significant negative impact on quality of life. Among women of reproductive age, signs and symptoms of excess estrogen relative to progesterone include decreased sex drive, irregular or abnormal periods (including excessive bleeding), bloating, breast swelling and tenderness, mood swings (especially irritability and depression), weight gain, cold hands and feet, and premenstrual headaches.
While compounds such as calcium-d-glucarate and di-indolylmethane (DIM)are effective for reducing estrogen levels, other interventions may be needed to boost flagging progesterone levels. Younger women may benefit from exogenous progesterone for the treatment of dysfunctional uterine bleeding resulting from anovulatory cycles, and progesterone may also be beneficial forendometrial hyperplasia due to chronic unopposed estrogen.
As for post-menopausal women, the natural decrease in progesterone levels that occurs with aging may result in hot flashes, mood swings, urinary incontinence, hair loss, vaginal dryness, poor concentration, uterine fibroids, loss of libido and an overall decline in health and quality of life.Additional symptoms include trouble sleeping, brain fog, and others that overlap with symptoms in younger women: breast tenderness, mood swings, water retention, and weight gain. Fortunately, many of these unpleasant and in some cases debilitating symptoms may be improved through restoration of healthy progesterone levels.
Google Dr.Malcom Kendrick–he offers an enormous format of information on Statin Drugs
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
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.
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.
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
“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
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.”
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 report8,9 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
“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.”
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
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,
“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
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
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.”
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
“… [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.”
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
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
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,21statins 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.
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
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
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
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
Rosacea is an inflammatory skin disease with an elusive pathology
that is thought to include a combination of microorganisms, genetic
predisposition, abnormal neurological signaling, a disrupted innate
immune system, and dysbiosis. The clinical presentations can differ
slightly between individuals and help classify rosacea into one of four
subtypes: erythematotelangiectatic, papulopustular, phymatous, and
Traditional therapy has focused on anti-inflammatory antibiotics, but
long-term pharmaceutical therapy is rarely a desirable option due to
the risk of gastrointestinal distress and antibiotic resistance. It is
also well known that there are specific triggers that exacerbate rosacea
including heat, sun exposure, spicy foods, alcohol consumption,
exercise, and heightened emotions. Given the fact that none of these are
modulated by antibiotics, questions are raised regarding other
treatment modalities that may more effectively address the underlying
causes of rosacea. Diet is increasingly becoming the focus as we learn
more about the gut-skin axis and its influence upon many of the elements
of rosacea including the microbial, inflammatory, and immune
Diet is unquestioningly becoming an aspect of managing all subtypes of rosacea. According to a survey by the National Rosacea Society,
78 percent of the 400+ patients surveyed had altered their diet due to
rosacea; and of this group, 95 percent reported a reduction in flares.
Of the dietary triggers reported in this survey, most fell into 4
groups: heat-related (hot coffee, tea), alcohol-related (wine, hard
liquor), capsaicin-related (spices, pepper, hot sauces), and
cinnamaldehyde-related (tomatoes, citrus, cinnamon, chocolate). One
explanation for the triggering effects of these foods is their ability
to stimulate vanilloid channels which are active in patients with rosacea.
When these channels are activated, they increase blood flow to the skin
via neurogenic vasodilatation, which causes the flushing and burning
associated with this condition.
In a multicenter retrospective case-control survey
of 2637 subjects (controls and patients with rosacea) that sought to
find a relationship between diet and rosacea, a high-frequency intake of
fatty food and tea was associated with rosacea, while a high-frequency
of dairy products negatively correlated with it (and may have actually
been linked to a reduction in rosacea severity).
The gut-skin axis is another explanation for the link between diet
and rosacea. Anecdotally, many patients with rosacea also experience
gastrointestinal conditions. A population-based cohort study
of nearly 50,000 Danish patients with rosacea discovered a high
prevalence of celiac disease, Crohn’s disease, ulcerative colitis, Helicobacter pylori
infection, small intestinal bacterial overgrowth (SIBO), and irritable
bowel syndrome. Research has already confirmed a direct link between the
microbiome of the gut and the robustness of the immune system.
Additionally, since the body’s inflammatory response is a role of the
immune system, these cannot be treated separately. Therefore, it should
be no surprise that rosacea – a condition with immunological and
inflammatory-based pathology – is also associated with gastrointestinal
conditions that are rooted in an unhealthy microbiome. This association
is further strengthened by the fact that antibiotics often lead to
short-term improvement but are not a long-term solution. Initially,
antibiotics eradicate the pathogenic organisms from the gut, but without
adequate probiotic and dietary support to rebuild a healthy microbiome,
the positive effect of the antibiotics diminishes and eventually has an
opposing effect on the gut.
The microbiome of the gut has also been shown to influence the
microbial composition of the skin, which may affect the bacterial
component of rosacea. Further, the skin microbiome modulates the immune
response at the surface of the skin. Since the pathology of rosacea
involves a dysregulated innate immune response, including enhanced expression of toll-like receptor 2 in the epidermis of rosacea patients,
correcting the gut microbiome may be a foundational process for
rebalancing the microorganisms and immune response of the skin.
Dietary patterns that support a balanced microbiome include 1)
fermented, probiotic-rich foods such as yogurt, kefir, miso, kimchi, and
sauerkraut; 2) dietary plant fiber to serve as prebiotics; and 3)
cold-water fish and seafood, and/or omega-3 fatty acid supplements as
substrates for anti-inflammatory prostaglandins that competitively
inhibit pro-inflammatory pathways. Low-carb, high-protein diets, such as
a Paleolithic diet, have been shown to positively modulate the
microbiome since they eliminate sugar sources that foster the growth of
pathogenic bacteria while providing nutrients that modulate the
inflammatory response and promote a favorable environment for beneficial
Individuals suffering from rosacea often groan as the summer months
progress since the heat and sun often exacerbate the flare-ups; however,
rosacea is far less of a seasonal problem and more of a year-round
gastrointestinal problem, meaning its management needs to begin with a
closer look at the diet.
Here are a list of Iodine links that I feel you should read and save in your Dr. Princetta file.
My position on breast cancer is to take matters into your own hands so as to prevent breast cancer at all cost.
In a nutshell,
Iodine decreases the
ability of estrogen to adhere to estrogen receptors in the breast
should get our nutrients from food. Seaweeds have the highest Iodine
content but unlike the Japanese, American do not eat seaweeds such as
Wakame, Kombu or Dulse. I am attaching a list of foods high in Iodine to
Because you cannot depend on diet alone to provide Iodine, I recommend the best products available such as:
1. Edgar Cayce Detoxified Iodine: 2-4 drops in water once or twice daily
2. Iodoral 12.5 mg: 1 per day x 3 weeks then 1 tab 3x weekly–decreasing gradually
3. Dr. Carolyn Dean’s Re-Myte (12 minerals; 9 of which are thyroid specific)
Here are the links I think you should take a look at: