Why there’s always hair in the shower, and what she can do about it
Hair loss in women is a frequent complaint in the family doctor’s office: it can begin in the early 20s and by age 30, it becomes a problem for 30%: men aren’t the only “suffferers”!
However the pattern of scalp hair thinning is different in the female: rather than an even line along which hair growth recedes, women’s hair tends to become uniformly thin: they don’t develop a “bald patch” but the thick, healthy hair growth of the teenager becomes generally thinner in the third decade, producing a “worn-out” appearance which is psychologically distressing.
The cause may be genetic (female pattern baldness); it may be hormonal (PCOS, thyroid issues, postnatal), or may seem to result from stress. Occasionally, it may relate to dietary deficiencies of iron, Vitamin D, Iodine, Selenium or other items.
In my practice, early hair loss was almost always accompanied by Brittle fingernails, anxiety, foggy thinking, hoarseness, dry skin and / or other hypothyroid symptoms.
The symptoms of DHEA deficiency, in females
Of 359 women, seen from 2006 to 2015, 335 (93.31%) were deficient in DHEA. Only 24 (6.68%) had a normal DHEA level (>6.0), when first seen.
Symptoms
As the chart below shows, the most frequent symptoms among my 359 female patients, were Hair loss and brittle nails, Fatigue, Brain Fog and low libido. Of these symptoms however, the most obvious. hair loss (universally accompanied by brittle nails), was the major source of distress.
Frequency of symptoms, as a percentage, among 359 women
Subscribe to continue reading
Subscribe to get access to the rest of this post and other subscriber-only content.
Supplementation, to achieve hormone balance, can be magical
STRESS, NCDs, AF, IH and body temperature
The prevalence of NCDs, including Atrial fibrillation (AF), rises with stress. Intracellular Hypothyroidsm (IH, aka Low T3 Syndrome, or LT3S), is a state of T3 deficiency in the serum. T3 deficiency causes paralysis of the brown fat, with resulting reduction of body temperature.
The graph below shows Stress and NCD deaths, increasing between 1960 and 2020. It also shows that while NCD deaths increase with stress, human body temperature falls, which is evidence of IH.
This graph shows Stress and NCD deaths, increasing between 1960 and 2020. NCD deaths increase, but body temperature falls: low temperature = IH.
What causes AF?
As Dr Y. P. Saleeby has just reminded us, AF is associated with a number of conditions: structural heart changes (anything that stretches, scars, or remodels atrial tissue can trigger A Fib): the condition tends to occur in tandem with Hypertension, Coronary Artery Disease, prior MI, Heart Failure, Valvular disease, Congenital heart disease, Cardiac surgery, Atrial enlargement or fibrosis and as a progression from “multiple extrasystoles”, which, when unaccompanied by other aberrations, is generally regarded as a benign condition.
To my mind, the increasing prevalence of AF is a manifestation of the general trend to rising incidence of NCDs, which has been documented over the past decades and therefore, is not remarkable in itself.
As to the question of aetiology of AF, “no-one knows”: but that we should remember that the condition can result from aberrations of hormonal balance, particularly deficiencies of DHEA, Testosterone and Progesterone and aberrations of thyroid hormone balance: Here are a few references (there are many more):
DHEA
In the Rotterdam study, “subjects in the highest DHEAS quartile had an almost three times lower risk of atrial fibrillation during follow-up, compared to those in the lowest DHEAS quartile (HR: 0.34, 95% CI: 0.18-0.64) adjusted for age, sex and cardiovascular risk factors.” In my favourite anecdote, Herman and Herbert, non-obese men of about the same age (65 & 66), developed Multiple Extrasystoles (“MEs”). Herman took DHEA and was fine: Herbert wouldn’t take it and he went into AF, about a year later!
Herman had MEs, took DHEA & was fine ……………………………………… Herbert had MEs, refused DHEA & got AF, then ablation, then stents, then a bypass, then a pacemaker and now, takes MULTIDRUGs
This is important: DHEA synthesis falls by 1% per annum after age 25, so everyone over 40 is DHEA deficient (+- a few exceptions, like Polycystic Ovarian Syndrome).
Subscribe to continue reading
Subscribe to get access to the rest of this post and other subscriber-only content.
AMBIENT CO2 IN RELATION TO METABOLISM: the coming rise in LT3S and NCDs
Ambient CO2, 428ppm, rises 3%/year. It is a factor in LT3S and in NCDs. WE MUST REDUCE OUR CARBON FOOTPRINT, or ACCEPT THE CONSEQUENCES
To Professor, Dr. Ugo Bardi:
Hi Ugo, I’ve just read your excellent, incisive paper on atmospheric CO2 levels, which you posted on 6th August, 2025 – I wish that I had gotten onto it sooner: please accept my apologies! Your point, based on cogent logic, that human metabolism can be adversely affected by increased ambient CO2, is well taken.
The implications got me thinking: I looked it up with AI and in corroboration, the machine replied:
Re. CO2s effect on metabolism
“Elevated ambient CO₂ impairs human metabolism by subtly shifting acid–base balance, increasing systemic inflammation, altering hormone‑regulated processes, and degrading cellular energy efficiency, even at concentrations far below those associated with acute toxicity.
The most consistent findings involve impaired cognitive metabolism, increased oxidative stress, and disruptions in calcium, bone, and kidney physiology.”
The conundrum and the emergency
With this in mind, our scientists should recognise, and consider, our current conundrum and our potential future emergency.
The conundrum, an ongoing reduction in body temperature worldwide, suggests an already-pervasive epidemic of Brown Fat paralysis, due to the stress-related low T3 Syndrome (LT3S)…… Dr. Denis Wilson was right! (see also, another post, re WTS)!
The emergency to be expected is a deepening of our endemic LT3S, as rising ambient CO2 increases the stressful metabolic aberration to which you refer. The situation is complicated by the propensity of deep LT3S to produce, eventually, a wide range of “autoimmune” diseases, a short list of more acute illnesses (including simple heart failure, Takotsubo cardiomyopathy and myxoedema) and psychocognitive effects, including deep depression and rapid-onset dementia.
This information is ominous, in view of the 3% P.A. rise in atmospheric CO2!
CO2s effect on human metabolism
As to its direct effect on our metabolism, the question is “over my head”, excepting that I am familiar with the effects of IL 6 and other cytokines. However on the basis that ANY stress, as judged by the Hypothalamus, leads to ACTH-induced Cortisol release, with an adverse effect on Thyroid-4 conversion to Thyroid-3, I must conclude that a further increase of atmospheric CO2, from its current level of 428ppm, must soon become important: the current CO2 level is already “important” – it could well be a factor in our worldwide stress epidemic, today.
Regarding that, I must remind you that the Low T3 Syndrome (LT3S) can reach catastrophic severity with few symptoms, can fail diagnosis and can persist subclinically for years, eventually presenting as an autoimmune problem of one sort, or another.
A large-scale study would perhaps, prove the point
It would be interesting to conduct a large-scale investigation of current “raw” FT3, rT3 and FT3/rT3 values – I would expect an almost across-the-board finding of T3/rT3=<20, diagnostic of LT3S (aka “Non-thyroidal illness” (NTIS), “Euthyroid Sick Syndrome” (ESS), and “Subclinical Hypothyroidism”), which I prefer to term “Intracellular Hypothyroidism” (”IH”), since that term best describes the metabolic aberration.
If a significant prevalence of low (<20.0) T3/rT3 ratio were found in the population, it would prove the presence of endemic IH and we would have to accept that the situation is potentially eco-threatening, already: it would become obvious, even to our oblivious politicians, that we MUST reduce our world’s atmospheric CO2 !!
A smaller study, on mice, perhaps?
Come to think of it, a smaller experiment might provide insight and a worthwhile lead: a study of mice, comparing FT3/rT3 ratios between those living in ambient air and those in a high-CO2 environment, would lend credibility to the question of investigating humans.
That’s where scientists, such as yourself, come in: I am a Non- academic “nobody”, with no Institutional connections and I am retired, to boot, so all I can do is suggest!
NOTES FROM AI
Readers familiar with my substack will already have the information below; but the unfamiliar may have difficulty believing and crediting it, so I consulted AI, the modern guru, to lend my words some modern-day credence!
Subscribe to continue reading
Subscribe to get access to the rest of this post and other subscriber-only content.
