Let's Work Together To Create A Working HairLoss Regimen

[wealthofwisdom]

did it stop your shedding?

At the time yes it did. I stopped taking everything that anybody had ever mentioned caused them hair loss or shedding and the major scary shedding stopped.

 

[ursidae]

It's simple. Because they never had MPB or they haven't regrown any hair actually. Same with Danny Roddy - he claims that he had MPB and beat it with diet, yet he can't provide any pictures. This mentality " I had regrowth, but I'm not going to provide pictures" is so anti-science... We should all aim to have theories with proof and reproducible results, not based on anectodal evidence. Internet is full of liars.

Danny Roddy looks to me like he was always extremely healthy

 

[DhtAssassin]

A simple google search of whatever it is plus "hair loss" (ie "vitamin a hair loss") will show you if articles, studies or personal stories have been written about it. It doesn't take a rocket scientist. Then you can read them and make your own decisions about if you believe them or not.

Since when personal story is a reliable source? If you believe in personal stories, then earth is flat and 5g causes corona. Research is number one priority, then sometimes you can add some anecdotal evidence. If it's only anecdotal - same as nothing.

 

[Vins7]

for me healthy nails= healthy hair and strong nails for me come from milk, eggs, and meat (i think b12 has a big thing to do with it). nails should be strong and have a nice pink tone i think.

What foods do you eat to get magnesium?

 

[gaze]

What foods do you eat to get magnesium?

milk orange juice (or any ripe fruit) and decaf and caffeinated coffee. The decaf instant coffee is helpful cause I can put more coffee into milk for magnesium then I could usually handle if it all had caffeine.

 

[johnwester130]

I've not been following hairloss/regrowth for a while cuz I'm at NW5/6 and I believe there's no point for me, but great idea for a thread hope it does well. I think I saw someone say Dr Peat mentioned Tabasco/Hotsauce topically, sounds crazy but I wonder how effective it is.

the hot sauce, or cayenne, is scientifically shown to convert white to brown fat

bald men lack bronw fat

beta lapachone also does that

Beta-lapachone activates brown fat cells - Beta-Lapachone.com

 

[Kenny]

the hot sauce, or cayenne, is scientifically shown to convert white to brown fat

bald men lack bronw fat

beta lapachone also does that

Beta-lapachone activates brown fat cells - Beta-Lapachone.com

Very interesting. So how do brown fat cells relate to hair loss? I have never heard of them discussed in this context before!

 

[johnwester130]

Very interesting. So how do brown fat cells relate to hair loss? I have never heard of them discussed in this context before!

read the article

bald men lose brown fat in their scalp

 

[Kenny]

I think it would benefit all of us folk here interested in hair loss to redirect this thread

read the article

bald men lose brown fat in their scalp

So brown fat is protective to the hair follicle and balding men - more specifically overweight and older men - tend to be lacking in it.

Brown fat is lost due to a lack of blood flow according to the article. Hmm. I wonder if they are right that increasing brown fat levels in the localized balding areas will all the hair to regrow.

Is it actually possible target specific regions to increase brown fat?

 

[PaRa]

Maybe a dumb idea but what if brown fat in scalp would allow it to be warmer so more vasodilation and better blood flow ? (And vice versa)

 

[BetterCallSaul]

Maybe a dumb idea but what if brown fat in scalp would allow it to be warmer so more vasodilation and better blood flow ? (And vice versa)

Cold water/showers can help activate brown fat

 

[johnwester130]

I think it would benefit all of us folk here interested in hair loss to redirect this thread


So brown fat is protective to the hair follicle and balding men - more specifically overweight and older men - tend to be lacking in it.

Brown fat is lost due to a lack of blood flow according to the article. Hmm. I wonder if they are right that increasing brown fat levels in the localized balding areas will all the hair to regrow.

Is it actually possible target specific regions to increase brown fat?

cayenne pepper also may activate the brown fat

 

[Kenny]

cayenne pepper also may activate the brown fat

Cold water/showers can help activate brown fat

I feel like if cold water/showers had a noticeable effect on hair we would have known about that ages ago right? I'm not really feeling that one.

Do you think applying cayenne topically may be effective? Orally?

 

[PaRa]

Cold water/showers can help activate brown fat

Yes bc brown fat makes heat, and applying cold to it make it active and usefull for the body so helps develops and preserve it

 

[johnwester130]

Yes bc brown fat makes heat, and applying cold to it make it active and usefull for the body so helps develops and preserve it

skip to browning agents

Browning of white fat: agents and implications for beige adipose tissue to type 2 diabetes

 

[JDreamer]

The cold shower routine or dunking ones head in ice water has been tried already.

 

[GorillaHead]

Guys that article anout brown has zero scientific sources lol.

 

[Kenny]

Guys that article about brown has zero scientific sources lol.

I didn't examine their validity any, but I am pretty sure they had a few sources listed at the bottom of the page. Anyway there are bigger problems with this brown fat approach than the sources.

Brown fat is produced from white fat which is also depleted in balding scalps. DhT is known to erode subcutaneous fat, both white and brown. Trying to get white fat to turn brown - using that beta - lapachone drug, curcumin, cold temperatures or whatever - would be pointless unless we can restore white fat in those areas to actually derive brown fat from. If we are able to actually restore subcutaneous fat in balding regions then we can go ahead and focus on upping our brown fat levels there.

 

[Kenny]

I think excess cortisol-aldosterone- mineralocorticoid activation trough angiotensin system are main players in balding by cytokine activation and progressing to fibrosis. Focusing on TGF-β₁, which shuts off the anagen phase of the hair cycle, and 11β-HSD₁ expression should fix to the problem. Angiotensin 2 receptor (AT-1) is involved in the inflammation pathway.

Angiotensin - Aldosterone has been shown to upregulate TGF-β₁. DHT upregulates 11β-HSD₁ expression.

Cortisol synthesis depends on the enzyme 11β-HSD1 and it converts the inactive cortisone into the active cortisol.


RENIN-ANGIOTENSIN-ALDOSTERONE SYSYTEM AND HAIR LOSS PROCESS

Although hair follicles express almost a full set of RAAS-associated receptors, the role of this system in the regulation of hair growth has not yet been described.


The data describing serum ACE activity in patients with alopecia areata are not consistent; however, both of the studies performed to date have exploited relatively small groups (102, 103). Moreover, one study has shown that in patients with mild or moderate alopecia areata, ACE tissue activity is decreased in the epidermis, as well as in follicular epithelium and endothelium.


The role of RAAS in the hair loss process should be considered as highly possible due to reports linking to the intake of ACE-I to hair loss. Interestingly, discontinuation of ACE-I treatment or switching patients from ACE-I to ARB has resulted in hair regrowth. However, the mechanism of ACE-I-induced alopecia is unknown.


There are some studies indicating the potential role of aldosterone and MR in hair loss. Postnatal MR overexpression in keratinocytes in mice has resulted in delayed alopecia, hair follicle dystrophy, and abnormalities of the hair cycle, without alternation of the interfollicular epidermis. Moreover, clinical studies have shown that both male and female patients with androgenic alopecia have higher aldosterone serum levels. The mechanism underlying this process may be associated with the skin microinflammation found in those patients. Despite the potential role of aldosterone, there is only one study evaluating the influence of MR blockade on hair. This showed that spironolactone treatment reduced hair shaft size and weight resulting in softer, finer hair and a slower growth rate in patients with hirsutism. In this study, the action of spironolactone was mainly associated with its antiandrogenic activity. Nevertheless, the potential role of MR blockade cannot be excluded. View attachment 17546 View attachment 17547

JPP No 3/2019 article 01



Both aldosterone and cortisol have a similar affinity for the mineralocorticoid receptor. To prevent over-stimulation of the mineralocorticoid receptor by cortisol, 11β-HSD converts the biologically active cortisol to the inactive cortisone, which can no longer bind the mineralocorticoid receptor. 11β-HSD co-localizes with intracellular adrenal steroid receptors. Licorice, which contains glycyrrhizinic acid and enoxolone, can inhibit 11β-HSD and lead to a mineralocorticoid excess syndrome. Cortisol levels consequently rise, and cortisol binding to the mineralocorticoid receptor produces clinical signs and symptoms of hypokalemia, alkalosis and hypertension (i.e. mineralocorticoid excess).

11β-hydroxysteroid dehydrogenase is expressed in the central nervous system of aged individuals. It is essential in Hypothalamo-Pituitary-Adrenal Axis function. 11β-hydroxysteroid dehydrogenase also partakes involvement in the decline of conscious intellectual activity due to ageing.

11β-HSD1 is responsible for activating glucocorticoids while 11β-HSD2 is responsible for deactivating them.

11β-Hydroxysteroid dehydrogenase - Wikipedia


Mineralocorticoid overexpression is expressed in hyper-keratinization. Mineralocorticoid excess is due to cortisol. Elevated mineralocorticoid is the consequence of defective cortisol metabolism, thus implicating impaired 11β-HSD2 activity.

A syndrome of apparent mineralocorticoid excess associated with defects in the peripheral metabolism of cortisol. - PubMed - NCBI


The local renin-angiotensin-aldosterone system (RAAS) is fully expressed in the human skin at the mRNA and protein level. Local RAAS is known to play a regulatory function in epidermal proliferation, wound healing, scarring, cutaneous heating adaptation, and aging. There are also some indications of its role in the regulation of hair growth and sebum secretion. Impaired wound healing, skin diseases associated with diabetes, cancer development, psoriasis, and scleroderma may be related to changes in skin RAAS activity. Extensive research has shown that RAAS-modulating drugs can affect the skin when applied orally or topically, creating new therapeutic approaches against dermatological diseases.

https://www.researchgate.net/public...ayer_in_skin_biology_beyond_the_renal_horizon


Linoleic acid - Arachidonic acid – Iron (heavy metals) are involved in inflammation – lipid peroxidation – hair loss.

Our data suggest that iron overload increases both lipid peroxidation and TGF-beta1 expression, which together could promote hepatic injury and fibrogenesis.

Excess iron induces hepatic oxidative stress and transforming growth factor beta1 in genetic hemochromatosis. - PubMed - NCBI

Arachidonic acid is synthesized from α-linolenic acid derived from linoleic acid, an essential fatty acid, by the enzyme Δ6-desaturase. ... Cyclooxygenase is an enzyme that transforms arachidonic acid into endoperoxides which are used to synthesize prostaglandins, prostacyclin, or thromboxanes.

Arachidonic Acid - an overview | ScienceDirect Topics



Oxidative Stress in Ageing of Hair

Ageing of hair manifests as decrease of melanocyte function or graying, and decrease in hair production or alopecia. There is circumstantial evidence that oxidative stress may be a pivotal mechanism contributing to hair graying and hair loss.

Oxidative Stress in Ageing of Hair \


A hypothetical pathogenesis model for androgenic alopecia: clarifying the dihydrotestosterone paradox and rate-limiting recovery factors

AGA is the result of chronic GA-transmitted scalp tension mediated by pubertal and post-pubertal skull bone growth and/or the overdevelopment and chronic contraction of muscles connected to the GA. This tension induces a pro-inflammatory cascade (increased ROS, COX-2 signaling, IL-1, TNF-α, etc.) which induces TGF-β1 alongside increased androgen activity (5-αR2, DHT, and AR), which furthers TGF-β1 expression in already-inflamed AGA-prone tissues. The concomitant presence of DHT and TGF-β1 mediates perifollicular fibrosis, dermal sheath thickening, and calcification of the capillary networks supporting AGA-prone hair follicles. These chronic, progressive conditions are the rate-limiting factors in AGA recovery. They restrict follicle growth space and decrease oxygen and nutrient supply to AGA-prone tissues – leading to tissue degradation, hair follicle miniaturization, and eventually pattern baldness.

…

Summary of observations concomitant with pattern hair loss in AGA tissues:

Biological Androgen activity (5-αR2, AR, DHT) - AGA tissues express more 5-αR2 activity, AR activation, and DHT than non-AGA hair-bearing scalp tissues [7], [97], [98]. Observations of castrates and 5-αR2 deficient men suggest androgen activity is involved in AGA development

Inflammation Substances and signaling proteins (ROS, TGF-β1, IL-1α, IL-1β, TNF-α) -AGA tissues express higher activity of reactive oxygen species (ROS) [99]. ROS tends to increase in the presence of transforming growth factor beta 1 (TGF-β1), an androgen-mediated signaling protein expressed more highly in AGA-affected skin [59], [100]. Elevated cytokines such as interleukin 1 alpha (IL-1α), interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) may contribute to hair loss disorders such as alopecia areata [101], [102], are suspected to partially mediate hair cycling from anagen to catagen, and may also contribute to AGA [103], [104], [105]

Prostaglandins (PGD2) - Inflammatory prostaglandins are observed in AGA [23], particularly prostaglandin D2 (PGD2) [106]. PGD2 is elevated in human AGA tissues and inhibits hair lengthening in mice.

Microorganisms and byproducts (P. acnes, porphyrins) - One study observed porphyrins in 58% of pilosebaceous canals in those with AGA versus 12% in non-AGA controls [107]. Porphyrins are a byproduct of Propionibacterium acnes (P. acnes), a commensal microorganism found in the skin biome which colonize sebaceous ducts, ingests sebum, and are implicated in acute inflammation and acne onset [108]

Tissue remodeling: Fibrosis (perifollicular fibrosis, dermal sheath thickening) - Fibrosis develops concurrently with AGA. Studies have found that 37% of AGA sufferers showed significant inflammation and fibrosis surrounding thinning hair follicles (perifollicular fibrosis) [109], increased collagen deposition below AGA miniaturizing follicles [110], and a 2- to 2.5-fold enlargement of the follicle dermal sheath made up of dense collagen bundles [111]. Balding vertex and temple regions have a near 4-fold increase in collagen fibers, [112] and AGA-linked fibrosis may match AGA progression and patterning [67]

Blood vessel calcification - Autopsy anecdotes suggest that calcification of the capillary networks supporting AGA-affected follicles may coincide with AGA progression. Frederick Hoelzel reported this when removing the brains of cadavers, noting a relationship between capillary calcification and baldness patterning [35]

Sebaceous gland size - AGA sufferers have enlarged sebaceous glands and higher sebum production in affected hair follicles [77], [110], [113]

Vascularity (oxygen) - Transcutaneous oxygen in frontal scalp regions of AGA men is 60% of transcutaneous oxygen in non-AGA counterparts [31], implying microvascular deficiency in AGA tissues

APM - AGA progression coincides with APM degeneration and its replacement with fat below vellus hair follicles [114]

Bone (skull shape) - Researchers have noted an anecdotal relationship between skull shape and baldness patterning, even in newborns – whose skull shapes often show similarities to AGA-affected skulls and whose hair often grows in reverse order of AGA patterning as the cranium develops during adolescence [68]

Structural Tension GA - Scalp tension in the tissues above the GA appears to match the pattern and progression of AGA where the highest tension points correspond to the first places of AGA onset [57]. This stress may be (1) influenced by androgens, and (2) alter the inactive standby of AR co-activator Hic-5/ARA55 and androgen-mediated TGFβ-1. A study on a device to relieve scalp tension demonstrated visual hair loss improvements in 65% of patients within 3–12 months [32], implying that GA-related tension may contribute to AGA hair thinning

Muscular - A pilot study on botulinum toxin injections into the muscles connected to the GA showed an 18% increase in hair count in AGA patients over 48 weeks [74], implying that their chronic contraction may be part of AGA pathology

A hypothetical pathogenesis model for androgenic alopecia: clarifying the dihydrotestosterone paradox and rate-limiting recovery factors - ScienceDirect


Induction of transforming growth factor-beta 1 by androgen is mediated by reactive oxygen species in hair follicle dermal papilla cells

The progression of androgenetic alopecia is closely related to androgen-inducible transforming growth factor (TGF)-β1 secretion by hair follicle dermal papilla cells (DPCs) in bald scalp. Physiological levels of androgen exposure were reported to increase reactive oxygen species (ROS) generation. In this study, rat vibrissae dermal papilla cells (DP-6) transfected with androgen receptor showed increased ROS production following androgen treatment. We confirmed that TGF-β1 secretion is increased by androgen treatment in DP-6, whereas androgen inducible TGF-β1 was significantly suppressed by the ROS scavenger, N-acetyl cysteine. Therefore, we suggest that induction of TGF-β1 by androgen is mediated by ROS in hair follicle DPCs.

Induction of transforming growth factor-beta 1 by androgen is mediated by reactive oxygen species in hair follicle dermal papilla cells


Clove oil (eugenol) inhibited 97.3% lipid peroxidation and decreases TGF‐β1 expression

Expression of TGF‐β1 was increased significantly in the diabetic control group. However, eugenol treatment decreases this increased expression.

Results suggest that treatment with eugenol involved amelioration of diabetic nephropathy by decreasing TGF‐β1 expression.

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Clove oil inhibited 97.3% lipid peroxidation of linoleic acid emulsion at 15 μg/mL concentration. However, under the same conditions, the standard antioxidant compounds such as butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), α-tocopherol and trolox demonstrated inhibition of 95.4, 99.7, 84.6 and 95.6% on peroxidation of linoleic acid emulsion at 45 μg/mL concentration, respectively. In addition, clove oil had an effective DPPH scavenging, ABTS+ scavenging, superoxide anion radical scavenging, hydrogen peroxide scavenging, ferric ions (Fe3+) reducing power and ferrous ions (Fe2+) chelating activities.

Antioxidant activity of clove oil – A powerful antioxidant source - ScienceDirect



Multiple nutritional, environmental and lifestyle factors can directly affect hair follicles, to weaken and make them sensitive to the action of androgens. Hair loss can be corrected and hair growth can be improved by addressing these non-androgenic factors. Patients having hair fall, thinning, loss of volume and poor growth can be precursors to androgenetic alopecia. Recent research has shown that androgens inhibit hair growth through release of Transforming Growth Factor (TGF) ß1. Further study of this mechanism reveals that generation of Reactive Oxygen Species (ROS) induced by androgens leads to release of TGF ß1 and use of ROS scavengers can block the release of TGF ß1, explaining beneficial role of antioxidants in hair growth. The binding of ROS to intracellular proteins also causes hair loss by altering the protein structure, changing their immune recognition and converting them to new antigens targeted by inflammatory and immune systems. Calorie restriction and individual micronutrient deficiencies lead to a new process of intracellular destruction or autophagy before cell apoptosis, which could explain cessation of hair growth. Telogen is not a resting phase but now defined as active conservation of follicles under unfavorable conditions. Thus any stress, trauma, metabolic change or insult causes telogen. Micronutrients zinc, copper, selenium maintains immunity, control inflammation and preserve antioxidant activity of the cells. Vitamins A, C, D have a role in phagocytosis and antibodies maintaining resistance. Vitamin D3 modulates the hair-inductive capacity of dermal papilla cells. Vitamin and micronutrient deficiencies are prevalent among all the population of the world. Nutritive value of the foods has reduced over the years by 30%. Endocrine Disrupting chemicals are creating further damage to the hormonal balance of the body. All these can be countered by use of antioxidants and a well-planned nutritional program which will ensure strengthening and regrowth of hair follicles, without the use of Finasteride. https://www.researchgate.net/public...n_Hair_loss_and_Hair_Regrowth_Review_Articlen


Lisinopril-Induced Alopecia: A Case Report

The American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines consider angiotensin-converting enzyme (ACE) inhibitors as one of the mainstay therapies in the management of heart failure. The widespread use of ACE inhibitors has been associated with several notable adverse effects such as hyperkalemia and an increased serum creatinine. There are no previous reports of alopecia associated with lisinopril use; however, a few previous cases of alopecia associated with other ACE inhibitors exist. This report discusses a case of lisinopril-induced alopecia of a 53-year-old male presenting to our outpatient heart failure clinic with a chief complaint of a new onset of alopecia. Upon evaluation, it was suspected that the patient’s alopecia was likely medication induced by lisinopril; therefore, lisinopril was discontinued and switched to an angiotensin receptor blocker (ARB), losartan potassium. Alopecia resolved in 4 weeks after the therapeutic intervention.

SAGE Journals: Your gateway to world-class research journals


The beneficial effect of Ang-(1-7) in alopecia can be attributed to their vasodilation action on blood vessels (Santos et al., 2000). The vasodilation of arterioles present in the dermis improves irrigation of the hair follicles, increasing the supply of nutrients and oxygen. Thus, the cells of the hair follicle increase their proliferation, accelerating hair growth

US20150313829A1 - Topical formulations for the prevention and treatment of alopecia and inhibition of hair growth - Google Patents


TGF-β plays important roles in the induction of catagen during the hair cycle. We examined whether TGF-β2 could activate a caspase in human hair follicles. Using active caspase-9 and -3 specific antibodies, we found that TGF-β2 activated these caspases in two regions, the lower part of the hair bulb and the outer layer of the outer root sheath. In addition, we searched for a plant extract that can effectively suppress TGF-β action. We found that an extract of Hydrangea macrophylla reduced synthesis of a TGDβ-inducible protein. We confirmed that the extract has a potential to promote hair elongation in the organ culture system. Furthermore, it delayed in vivo progression of catagen in a mouse model. Our results suggest that the induction of catagen by TGF-β is mediated via activation of caspases and that a suppressor of TGF-β could be effective in preventing male pattern baldness.

A Potential Suppressor of TGF-β Delays Catagen Progression in Hair Follicles - ScienceDirect



Angiotensin II is also well known in inducing reactive oxygen species and promoting inflammatory phenotype switch via its type 1 receptor. In clinic, Angiotensin II type 1 (AT1) receptor blocker like candesartan has been widely applied as an antihypertensive medication.

It was found that pre-treat with candesartan significantly suppressed transforming growth factor-β (TGF-β) and interleukin-6 (IL-6) expression after incubation with TNF-α.

Candesartan inhibits inflammation through an angiotensin II type 1 receptor independent way in human embryonic kidney epithelial cells


Related to stress

Angiotensin II type 1 (AT(1)) receptors are expressed within organs of the hypothalamo-pituitary-adrenal (HPA) axis and seem to be important for its stress responsiveness. Secretion of CRH, ACTH, and corticosterone (CORT) is increased by stimulation of AT(1) receptors. In the present study, we tested whether a blockade of the angiotensin II system attenuates the HPA axis reactivity in spontaneously hypertensive rats.


Gene expression of AT(1A), AT(1B), and AT(2) receptors within the HPA axis was not altered by any drug. We show for the first time that antihypertensive treatment by inhibition of AT(1) receptors or angiotensin-converting enzyme attenuates HPA axis reactivity independently of blood pressure reduction. This action is solely evident after CRH stimulation but not under baseline conditions. Both a reduced pituitary sensitivity to CRH and a down-regulation of hypothalamic CRH expression have the potential to reduce HPA axis activity during chronic AT(1) blockade or angiotensin-converting enzyme inhibition.

Angiotensin II inhibition reduces stress sensitivity of hypothalamo-pituitary-adrenal axis in spontaneously hypertensive rats - PubMed

This was a phenomenal post. Thank you @md_a

 

[md_a]

“The reduction of parathyroid hormone by increased calcium and vitamin D is closely related to reduced obesity, and to the health problems associated with obesity-hypertension, insulin resistance, heart arrhythmias, depression, and various inflammatory conditions.
Surgeons will say many things to get customers, but one website promoting removal of enlarged parathyroid glands makes the interesting comment that they see an average of three women per day who are going bald from hyperparathyroidism.

"The longer they have hyperparathyroidism the more hair they lose" [https:// www.facebook.com/Parathyroid/photos/a] .

In vitro experiments with hair follicles show that parathyroid hormone ends the growth cycle. Prostaglandin D2, associated with hair loss, is released from mast cells, and parathyroid hormone is an activator of mast cell degranulation. Hair growth has a 24 hour cycle, and the long cycle of hair shedding and renewal seems to be regulated by the genes involved in the daily cycle (Lin, et al., 2009). It's possible that the daily cycle of parathyroid hormone is responsible for progressive hair loss, as it is for progressive loss of calcium from the bones; many people notice a copious loss of hair mainly in the morning. If this is the case, then a glass of milk at bedtime might have the same protective effect on hair loss that it has on bone loss.

Hair loss, like obesity or hypertension, should be taken seriously, as an indication of a systemic metabolic problem. The metabolism of the hair follicle contains clues to aging, tissue regeneration, and cancer. Milk contains multiple factors that lower parathyroid hormone, and other stress-related hormones.”

…

“Phosphate, which predominates in grains, beans, nuts, meats, and fish, increases our production of parathyroid hormone, while calcium and magnesium inhibit its production. This hormone, which increases with age, suppresses immunity, and in excess it causes insomnia, seizures, dementia, psychosis, cancer, heart disease, respiratory distress and pulmonary hypertension, osteoporosis, sarcopenia, histamine release, inflammation and soft tissue calcification, and many other problems.”

Ray Peat `Adaptogenic Milk`