salt migraine

Aimovig™: A Miracle Migraine Treatment or Unnecessary Risk?

39069 views

On July 31, 2018, the Daily Mail of London wrote about the Stanton Migraine Protocol and how a simple dietary change can help prevent migraines. The journalist became curious about the topic because a migraineur gave a testimonial about this protocol on YouTube. The paper started off with:

The conventional advice — backed by everyone from the NHS to the British Heart Foundation and the Scientific Advisory Committee on Nutrition — is to reduce salt intake where possible, owing to its links with high blood pressure, heart disease and stroke.

The official guidance is that we should eat no more than 6g of salt a day, which is around a teaspoonful. But Tracey, from Stretford, near Manchester, is one of a growing number of people following a controversial plan devised by a U.S. neuroscientist which involves eating twice that amount — with occasional extra scoops of ‘emergency salt’ — in a bid to keep migraines at bay

Thus, the topic of taking extra salt was critically viewed as a recognized health concern. The same article concluded:

However, there is now a preventive drug specifically developed for migraine called Aimovig.’ This has just been approved by the European Medicines Agency and ‘should soon be on prescription from GPs’.

The Migraine Trust advises consulting a GP first if you are considering consuming more salt.

Let me spell out what these quotes demonstrate exactly. Currently, most medical professionals consider taking a brand-new drug safer than taking of a bit of extra salt.

Salt and Health

Salt is in every human cell taking up about 0.4% of the body’s weight and is an essential mineral for survival. We lose salt by sweating, talking, breathing, and by our internal toxin removal processes making daily salt consumption essential for remaining healthy. The 6 gr salt amount recommendation by the above mentioned agencies and the USDA has been debated to be too low for health for years. For instance, an article in the academic journal The Lancet found that about 10 gr salt (4 gr sodium) is the ideal amount for those with heart events and even more for those whose hearts are healthy1. It also shows that at 3 gr salt (1.2 gr sodium) or less per day, an individual’s health takes an exponential turn for the worse and fatalities may occur. A Headache journal article found that there is an inverse relationship between salt consumption amount and migraine—meaning increased dietary sodium reduces the occurrences of migraines2.

I have yet to see the claim “essential” placed on a medicine, yet without hesitation many medical professionals view medicines a safer option than an essential mineral we must consume every day.

Medicinal Migraine Treatments

Migraine is a very painful and disabling condition that about 15% of the population endures, often daily, for many years. Up until now, there have been no migraine preventive medications on the market and migraine sufferers are prescribed a host of dangerous medications, cocktails of them, originally intended for other health conditions.

  • Anticonvulsants (anti-seizure medications)—Topamax, Neurontin, or Lyrica;
  • Tricyclic antidepressants (simple serotonin)—Amitriptyline or Nortriptyline;
  • SSRIs (selective serotonin reuptake inhibitors)—Lexapro or Zoloft;
  • Beta blockers or ACE inhibitors—Propranolol or Toprol;
  • Opiates—codeine, fentanyl, hydrocodone;
  • Anti-inflammatory—Corticosteroids;
  • NSAIDs—Celebrex;
  • Triptans—Imitrex, Frova, Maxalt, etc.;

The universal complaint from migraineurs across the board is that none of these medicines works and that they have debilitating side effects. Will Aimovig™ be different and help migraineurs? And, more importantly, will it be safe?

Aimovig™

Aimovig™ (AMGEN, Novartis) was approved by the FDA as the first migraine preventive medicine on May 17, 2018. The medicine is a CGRP receptor agonist. CGPR stands for Calcitonin Gene-Related Peptide Receptor. Calcitonin gene-related peptides have major roles in the central nervous system (CNS) and throughout the body. CGRP is a protein that modulates a variety of physiological functions, such as respiratory, endocrine, gastrointestinal, immune, and cardiovascular function. CGRP also affects the thyroid. Calcitonin acts to reduce blood serum calcium, and thus blocking it, would likely increase serum calcium. The increase in serum calcium is undesired. Too much calcium in the blood can weaken bones, and participates in atherosclerosis, which is the calcification of the arteries, causing hardening—this is referred to as coronary artery calcification.

Some nerve blockers, like Botox, have been demonstrated to block CGRP as well. CGRP modulates cyclic adenosine monophosphate cAMP, a messenger that is important in many biological processes. It is a derivative of ATP and used for intracellular signaling. CGRP is a potent hypotensive peptide—it is a vasodilator3.

CGRP blockers work by reducing stimulus that would reach nociception. Nociceptors detect noxious or harmful stimuli everywhere in the body and signal this stimulus by pain. Aimovig™ specifically targets nociceptors and prevents them from discovering harmful stimuli.

In some conditions, excitation of pain fibers becomes greater as the pain stimulus continues, leading to a condition called hyperalgesia” (see here).

Hyperalgesia means that the receptors become increasingly sensitive to pain over time (see here). For example, opioid-induced hyperalgesia may develop as a result of long-term opioid use4. This suggests that long term use of Aimovig™ may also induce hyperalgesia. This was not studied in the clinical trial. CGRP blocking may pose a risk in subjects with comorbidities such as cardiovascular diseases.

It is important to recall how SSRIs work (see my previous article on how inhibitory systems can cause life threatening health conditions by permanently blocking channels), because it appears that Aimovig™ acts similarly. A journal article describes the findings on Aimovig™ (there labelled as Erenumab/AMG334) alongside with other anti-CGRP monoclonal antibody trials by other pharmaceuticals. The research data of the clinical trial was released to the scientific community with an appendix providing the details. one can also get a pretty good idea of the information the FDA considered or received to be considered from the FDA label and from descriptions of competing products for which the information was released5,6.

Aimovig™—The Label

At the Aimovig™’s website, there is a video of slide presentation for healthcare professionals, from which I created a transcript. You can find the slides on this page.

  • CGRP signaling plays a key role in migraine pathophysiology by modulating nociceptive signaling within the trigeminovascular system.
  • Aimovig™ is a 100% human monoclonal antibody designed to help prevent migraine by targeting and blocking the CGRP receptor
  • Aimovig™ binds to the CGRP receptor and antagonizes CGRP receptor function
  • “Although the exact role of CGRP in migraine has yet to be determined, compelling evidence supports its involvement. First, CGRP levels have been shown to increase significantly with migraine and decrease with headache relief post sumatriptan treatment. Second, intravenal infusion of CGRP induces migraine-like headache in migraine patients, demonstrating that CGRP may play a causal role in migraine.
  • Prior to the study, participants who have not received any benefits from other migraine treatments (categories listed above) were excluded from the study.
  • In Studies 1, 2, and 3, 1.3% of patients treated with Aimovig™ discontinued double-blind treatment because of adverse events. Although only injection site irritations are reported by the FDA, the study indicates additional adverse effects, such as cold, upper respiratory tract infection, ankle fracture, viral gastroenteritis, sepsis, colitis, vestibular neuronitis, backpain, migraine, ovarian cyst, and sinusitis. One person also experienced cerebral venous thrombosis (see table 3). The most frequent injection site reactions were injection site pain, injection site erythema, and injection site pruritus—as per the label. Interesting to note that constipation and site irritation are listed as side effects on the label.
  • As with all therapeutic proteins, there is potential for immunogenicity. (Immunogenicity is the ability of a particular substance, such as an antigen or epitope, to provoke an immune response in the body of a human and other animal. In other words, immunogenicity is the ability to induce a humoral and/or cell-mediated immune responses; source Wikipedia) “A total of 35 of the 628 patients (5.6%) for whom postbaseline antibody data were available tested positive for anti-erenumab binding antibodies (8.0% of patients in the 70-mg group and 3.2% of patients in the 140-mg group), one of whom, in the 70-mg erenumab group, tested positive for neutralizing antibodies (0.2%)” (see here under SAFETY)
  • In controlled studies with AIMOVIG, the incidence of anti-erenumab-aooe (the main ingredient in Aimovig) antibody development was 6.2% (48/778) in patients receiving AIMOVIG 70 mg once monthly (2 of whom had in vitro neutralizing activity) and 2.6% (13/504) in patients receiving AIMOVIG 140 mg once monthly (none of whom had in vitro neutralizing activity). The neutralizing anti-erenumab-aooe antibody positive rate may be underestimated because of limitations of the assay (emphasis added by me)
  • Antibody development on the efficacy or safety of AIMOVIG in these patients, the available data are too limited to make definitive conclusions.
  • Erenumab-aooe is produced using recombinant DNA technology in Chinese hamster ovary (CHO) cells.
  • Erenumab-aooe exhibits non-linear kinetics as a result of binding to the CGRP receptor (something scary).
  • The effective half-life of erenumab-aooe is 28 days (ouch! If it harms you, just to get to half the dose you need to wait a month!)
  • The carcinogenic potential of erenumab-aooe has not been assessed.
  • Genetic toxicology studies of erenumab-aooe have not been conducted.
  • Mating studies have not been conducted on erenumab-aooe (may not be safe while pregnant).

Aimovig™— The Efficacy

This is a fascinating part because, while it is believed by most that a clinical trial is always meaningful and honestly reported on, here we have an example of a misleading clinical trial summary. There were three clinical trials, all of them examined the number of migraine-free days gained using Aimovig™ compared with taking a placebo. The label, which lists all clinical trial details, chooses to ignore a few important factors. For example, they report reduction in migraine days for only those subjects for whom Aimovig™ provided reduction, yet in the three studies, not one exceeded 50%–meaning it did nothing for at least 50% of the participants. In the tables below where the reduction of migraine days is listed, it is only for those for whom the drug actually provided some benefits. It is important to note that in all of the three trials, migraineurs were able to use additional pain reduction agents on migraine pain days, clouding the information gained from Aimovig™’s usefulness or lack thereof. Here is a summary write-up for episodic migraine sufferers participating in the trial:

Between the start of the study and four to six months of treatment, in the 70-mg group, 43.3 percent of patients experienced at least a 50 percent reduction in the number of migraine days experienced each month.

Between the start of the study and four to six months of treatment, in the 140-mg group, 50 percent of patients experienced at least a 50 percent reduction in the number of migraine days experienced each month.

Between the start of the study and four to six months of treatment, in those receiving placebo, 26.6 percent experienced at least a 50 percent reduction in the number of migraine days experienced each month.

The number of days in which patients had to use specific medications to treat acute migraines was decreased by 1.1 days in the 70-mg group and 1.6 days in the 140-mg group as compared with 0.2 days in the placebo group (here)

Let’s examine the reports on the clinical trials—both episodic and chronic migraines, with or without aura. The first and second groups are episodic migraines, where episodic migraine is defined as <15 migraine days a month. These were randomized, multi-center, placebo-controlled, double-blind studies—the first one was for 6 months. Only 90% of those enrolled completed study 1. There are two treatment groups, one receiving one 70 mg injection once a month and the other receiving one 140 mg dose of injection once a month, and a third is placebo group.

They evaluated the success (called “end points”) after 4 months of Aimovig™ use for the three-month period from 4 – 6 months. The findings are as follows:

Migraine-free days gained Aimovig™ 70 mg Aimovig™ 140 mg Placebo
Change from baseline -3.2 -3.7 -1.8
Difference from placebo -1.4 -1.9
Responders 43.3% 50.0%
Nonresponders 56.7% 50.0%

Let me explain the bolded areas. The 56.7% at the 70 mg dose and 50% at the 140 mg dose represent the non-responding population that took Aimovig™ and had no benefits from the drug at all. Thus, the number of migraine-free days gained (number of migraine-days reduced) represents only those for whom Aimovig™ actually worked. And what was that difference? Less than two migraine-free days compared with the placebo. Given the definition of episodic migraine as <15 pain days a month, saving 1.4 days of pain day for 43.3% of the population means the migraineur still ends up with 12.6 migraine days for a person with normally 14 migraine pain days a month, and for those receiving the 140 mg dose, the reduction is 1.9 days so from 14 days they reduce to 12.1 migraine pain days. This is a rather modest decrease in migraine pain days of 4% for those in the 70 mg group and 6% for those in the 140 mg.

These percentages are derived as follows (for the 70 mg case): up to 1.4 pain-free days difference from placebo, representing (1.4/15) = 9.3%. With only 43.3% of the population gaining this benefit the actual benefit is 43.3% of the 9.3% or (0.093 x 0.433) = 0.04, that is 4% benefit for the whole population.

In study 2, a randomized, multi-center, 3-month, placebo controlled, double-blinded study with episodic migraine—very similar to the previous trial with only a dose of 70 mg once a month, patients were also allowed to use other medicines, like triptans when they had migraines. Here 95% of the participants completed the study.

Migraine-free days gained Aimovig™ 70 mg Placebo
Change from baseline -2.9 -1.8
Difference from placebo -1.0 (rounding on label and not by me)
Responders 39.7%
Nonresponders 60.3%

Note here the responders were even fewer, meaning only 39.7% of the subject received any benefit from Aimovig™, and only gained 1 pain-free day compared with placebo. Given that the definition of episodic migraine is <15 pain days a month, saving 1 day for 39.7% of the population amounts to a 2.65% benefit. A very modest decrease in pain days since the number of pain-days remain at 13 for a person with an average of 14 pain-days a month.

The third clinical trial was with chronic migraineurs, which is defined as >15 pain days a month.

Migraine-free days gained Aimovig™ 70 mg Aimovig™ 140 mg Placebo
Change from baseline -6.6 -6.6 -4.2
Difference from placebo -2.5 -2.5
Responders 39.9% 41.2%
Nonresponders 60.1% 58.8%

In the chronic migraine group we find the least number of responders. While the migraine-day reduction is 2.5 compared with the placebo, we must remember that in chronic migraine, the pain days are greater than 15.  Assuming 16 pain days to be more than fair, saving 2.5 days a month for 39.9% of the population in the 70 mg group amounts to 12.5 migraine-pain days still left and thus the total benefit is 6%, and for those on 140 mg the benefit amounts to 6.4%. Of course, these benefits drop as pain days increase. For a migraineur with 20 pain days, these benefits drop to 5% because she still only gains 2.5 migraine-free days, while the actual migraine-days remain high at 17.5 days. This sort of benefit is of no benefit at all.

Aimovig™ Or Salt?

Given how incredibly little benefits Aimovig™ provides to less than 50% of migraineurs, and with so many unknowns about the possible adverse effects with long-term use, I must wonder: would I ever consider taking a drug like this?

As a migraine sufferer myself, I can reach complete migraine-free status by adjusting what I eat and by increasing my salt consumption. I would never ever consider a drug like this.

Do I need my doctor’s permission to increase my salt intake, as suggested by the Daily Mail? I don’t think my doctor would be very happy if I contacted him every time I used my salt shaker for more salt. Besides, I have increased my salt consumption to be several times greater than the USDA recommendation and while I certainly have no migraines, my blood pressure has never increased either. Salt doesn’t increase blood pressure and for most people there are no risks associated with consuming salt.

Taking any medication always carries the risk of side effects and interactions. Given the miniscule benefits of Aimovig™ as outlined above and the availability of a proven, non-medicinal treatment for migraines, is the enthusiasm for this drug warranted by the facts? What do you think?

Sources

  1. Mente, A. et al. Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies. The Lancet 388, 465-475, doi:10.1016/S0140-6736(16)30467-6 (2016).
  2. Pogoda, J. M. et al. Severe Headache or Migraine History Is Inversely Correlated With Dietary Sodium Intake: NHANES 1999–2004. Headache: The Journal of Head and Face Pain, n/a-n/a, doi:10.1111/head.12792 (2016).
  3. Tortorella, C. M., Carlo; Fornesis, Myriam; Nussdorfer, Gastone G.;. Calcitonin gene-related peptide (CGRP), acting via CGRP type 1 receptors, inhibits potassium-stimulated aldosterone secretion and enhances basal catecholamine secretion from rat adrenal gland. International Journal of Molecular Medicine 8, 4, doi: https://doi.org/10.3892/ijmm.8.3.261 (2001).
  4. Chu, L. F., Angst, M. S. & Clark, D. Opioid-induced Hyperalgesia in Humans: Molecular Mechanisms and Clinical Considerations. The Clinical Journal of Pain 24, 479-496, doi:10.1097/AJP.0b013e31816b2f43 (2008).
  5. Bigal, M. E. et al. Safety, tolerability, and efficacy of TEV-48125 for preventive treatment of chronic migraine: a multicentre, randomised, double-blind, placebo-controlled, phase 2b study. The Lancet Neurology 14, 1091-1100, doi:10.1016/S1474-4422(15)00245-8 (2015).
  6. Dodick, D. et al. Randomized, Double-blind, Placebo-controlled Trial of ALD403, an anti-CGRP peptide antibody in the prevention of chronic migraine. (S52.003). Neurology 88 (2017).

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

Image credit: Angela Stanton

This article was published originally on August 8, 2018.

Share

Migraine Brain as a Survival Advantage: Connecting the Dots with Angela A. Stanton

4882 views

On February 2nd, 2017, Thursday morning at 10 am Central time, I will be on ONE RADIO NETWORK (see schedule here). On this talk show I will present my views about the causes of migraines. The talk show invites advance emailed-in questions to email@oneradionetwork.com, as well as live call-ins during the show at: 888.663.6386. Here is the page where you can listen to the archived recording on the Internet (one hour talk show). If you are in Austin, Texas, you can listen on the radio.

Migraine Brain as a Survival Advantage

For a while we have known that the human body contains approximately 20 thousand genes, although this number seems to be a moving target as technology improves. The latest studies have reduced it to 19 thousand. From the 19 thousand, so far 1254 genes have been associated with migraines. Such a huge number of genes – associated with a condition that plagues nearly 30% of the population – begs for an explanation.

Could it be that migraine at one time in human history provided a survival advantage? A benefit that helped those endowed with this set of genes to survive? The answer to this question must be “yes” because the migraine-brain has survived in the population for so long. It has not been bred out of human populations over the millennia of our evolution. Health conditions disadvantageous for survival normally get deleted from our genome.

The question “why migraine hurts” has a simple answer based on this theory: pluck a group of people with a special adaptation from its natural habitat and place it into a different environment, and what was an advantage suddenly becomes a disadvantage. There are many examples for this in nature.

Greenland Inuit, Canadian Inuit and the Native American populations all have glucose (simple sugar into which all carbohydrates, including fruits and vegetables, grains, nuts, seeds, and some percent of proteins convert) intolerance genes. Fructose (a sweet substance that is approximately half of table sugar; found in fruits, vegetables, and syrups like honey, maple syrup, and of course high fructose corn syrup) can also be problematic. Many of us are born without the necessary enzymes to absorb fructose. The inability to digest sugar can cause diarrhea. In medical parlance, this is called “malabsorption” but the question remains: if so many people are born without the ability to absorb sugar, would that be considered a “malabsorption” or is sugar absorption an adaptation that occurred later in time?  I am not the first one to ask this question.

Now returning to migraine: it is found in at least as large fraction of the population as it is for the inability to absorb sugars, like glucose or fructose. The set of adaptations for the more sensitized brain to danger (that migraineurs today still possess) at one time may have been present in all of our predecessors. Some percent of the ancient population likely never lost this highly sensitized brain adaptation because in the ancient environment it would have provided a survival benefit. However, in our modern life, the highly sensitized brain has become a painful burden, whereas a large percent of the population adapted to modern life, reduced their brain sensitivity and they feel no pain. This is likely similar to how the majority of the population adapted to digest and absorb sugar; only a minority retained their inability to do so, and they still experience painful health conditions as a result.

The cause of migraines is not the pain—the pain is one of many symptoms. Just like medicating children to be able to eat an ice cream makes little sense, so is medicating migraine pain by blocking certain brain functions makes little sense. That is the only thing that the medicines are able to do and they are dished out to migraineurs like candy. Here are three of the most common (and most dangerous) medications given to migraineurs as “preventive” and what they block: Propranolol (blocks cardiac and neuronal voltage-gated sodium channels), Topamax (blocks voltage gated calcium and sodium channels), Amitriptyline (blocks or initiates many channels out of sync, causing major heart damage and sometimes death). Would we put ourselves at these types of risks in order to be able to eat a piece of sugar if we lacked the enzymes to digest them? I think the real problem is the lack of understanding of the true nature of migraines.

Migraines and Salt

Migraine starts with prodromes that are signals of an impending migraine. These prodromes precede a cascade of events that lead to the pain, which starts with the initiation of an alarm status that leads to fight-or-flight from danger. A migraineur can easily be triggered into a migraine by noise, odor, a specific light intensity, and even taste that is above or below the norm. Migraineurs have hyper sensory organ sensitivities (1), more sensory neuronal connections than the norm (2), and this is how perfume can trigger a migraine because that scent is above the norm. A migraineur will start a migraine unless voltage is re-established. Why voltage? Migraineurs use more voltage (3, 4) as a result of the more sensitive sensory organs. Voltage is generated by the sodium/potassium pumps that are located in cell membranes, facilitating voltage differential exchanges between the inside and the outside of the cell. Since more voltage use requires more salt, migraineurs need to consume more salt (sodium chloride). Migraineurs tend to pass more sodium in their urine as a result (5).

The modern Western diet is forever reducing its salt recommendation for the general population, ignoring that a large percent of that population needs more salt than what is recommended. In general, I found that migraineurs need approximately 50% more salt in their diet than non-migraineurs.

Migraines and Sugar

Another factor is sugar. While there is no academic research on migraineurs lacking enzyme to absorb fructose or that they are genetically lacking glucose absorption (although there are many research papers hinting at their possibilities–here is a review of some), it seems, based on the several thousand migraineurs I studied, that migraineurs are either sugar intolerant or are hyper sensitive to sugar—and all forms of carbohydrates. Indeed, migraineurs usually become insulin resistant. It would be quite educational to provide genetic testing to all migraineurs to find out what may drive their intense reaction to carbohydrates. Most migraineurs can completely prevent all migraines by completely avoiding refined carbohydrates, reducing complex carbohydrates to near the low carbs high fat (LCHF) diet levels, and increasing dietary animal fats (not oils).

Myelin is made from fat and cholesterol; it is the white matter in the brain, responsible for insulating the neurons’ axons, the parts that transmit voltage. Since migraineurs transmit voltage more often, their myelin is more likely to get damaged. Glucose seems to aggravate nerves in general in all central nervous systems conditions. The ketogenic (high fat, very low carbohydrate) diet may be ideal for migraineurs since it appears to repair the myelin damage glucose causes. Myelin can be replenished by eating a proper, high in natural fat (not man-made oils) diet and by ensuring that a migraineur retains a healthy insulin response. As expected, migraine is highly correlated with the incidence of insulin resistance (6-8), diabetes mellitus (7), obesity (9), and cardiovascular disease (10).

If migraine were a true disease, dietary changes would not be able to change the brain response in a way that all migraines become preventable and abortable without medications. Since they can be prevented and aborted with the proper migraine-brain diet (an ancient type diet that is void of simple sugars and complex carbohydrates in excess), it follows that migraine is an unintended consequence of the modern Western diet and it is not a disease.

Sources:

  1. Schwedt TJ (2013) Multisensory Integration in Migraine. Curr Opin Neurol:248-253.
  2. Tso AR, Trujillo A, Guo CC, Goadsby PJ, & Seeley WW (2015) The anterior insula shows heightened interictal intrinsic connectivity in migraine without aura. Neurology:1043-1050.
  3. Liu H, et al. (2015) Resting state brain activity in patients with migraine: a magnetoencephalography study. in The Journal of headache and Pain, pp 16-42.
  4. Tessitore A, et al. (2015) Abnormal Connectivity Within Executive Resting-State Network in Migraine With Aura. Headache 55(6):794-805.
  5. Campbell DA, Tonks EM, & Hay KM (1951) An Investigation of the Salt and Water Balance in Migraine. British Medical Journal:1424-1429.
  6. Bhoi S, Kalita J, & Misra U (2012) Metabolic syndrome and insulin resistance in migraine. The Journal of Headache and Pain 13(4):321-326.
  7. Guldiken B, et al. (2009) Migraine in Metabolic Syndrome. The Neurologist 15(2):55-58.
  8. Sachdev A & Marmura MJ (2012) Metabolic Syndrome and Migraine. Frontiers in Neurology 3:161.
  9. Bigal ME, Liberman JN, & Lipton RB (2006) Obesity and migraine: a population study. Neurology 66.
  10. Tana C, et al. (2013) New insights into the cardiovascular risk of migraine and the role of white matter hyperintensities: is gold all that glitters? The Journal of Headache and Pain 14(1):9.

We need your help.

Hormones Matter needs funding now. Our research funding was cut recently and because of our commitment to independent health research and journalism unbiased by commercial interests, we allow minimal advertising on the site. That means all funding must come from you, our readers. Don’t let Hormones Matter die.

Yes, I’d like to support Hormones Matter.

Share