The liver is an energy reservoir. It’s the main communication channel that tells the thyroid to produce hormones keeping the body in check. If the liver is impaired or stressed through various inputs (e.g. stress, poor diet, lack of sleep, etc.), the thyroid cannot receive the proper instructions for normalizing hormonal activity.

What ends up happening with a scrambled communication signal between the liver and the thyroid is an accumulation of anti-hair growth hormones as a result of thyroid disruptiveness. When both these important organs shut out, what is known as “The Hair Loss Avalanche” (all the events at the intercellular level leading up to hair loss) is at its greatest!

One of the early signs of hormonal imbalance due to an unhealthy liver is a change in the testosterone:estrogen ratio. The ratio is different for male and female victims of hair loss, so make sure you read the applicable following sections carefully.

For men, too much ESTROGEN, specifically estradiol (also known as E2 or 17β-estradiol), with too little testosterone elevates prolactin, which is bad for the hair. In this study[1], 65 males with androgenetic hair loss had elevated E2.

Furthermore, this mice study[2] solidifies the catastrophic effect of topical 17β-estradiol on the hair cycle. To save you time, I went ahead and laid out the three key findings:

1. Prolongs the catagen (regression) while sustaining the telogen (resting) hair phases
2. TGF-β2, a hair antagonist (bad), is upregulated in the dermal papillae causing the hairs to be stuck in catagen
3. BMP-4, a hair antagonist (bad), immediately increased after catagen further sustaining telogen and preventing a transition to anagen

The good news is the stem cells were still intact and alive in the dermal papillae and weren’t affected by application of 17β-estradiol. What that basically means is once estradiol was back to normal or no longer applied, because the stem cells are still present, dormant hairs have the capability of coming back to life. So long as the stem cells are alive, they are active, and can reproduce lifeless hairs.

To further shed estrogen’s carnage, it’s “venomous” behavior on hair growth were even notated as far back as 1958, in The Biology of Hair Growth.[3]

Don’t be fooled though, because there’s another side of the coin. A high estrogen:testosterone ratio is only one standard to consider if you’re a male losing your hair. It turns out, male pattern baldness can also arise from a high testosterone:estrogen ratio meaning testosterone is more prevalent than estrogen as this study[4] indicates.

On the contrary, women who have too little estrogen and too much TESTOSTERONE can experience the similar hormonal temperament as men as explained by Dr. Eric Berg.[5]

Dr. Berg’s explanation is further expounded by Yelva Lynfield’s experiment with pregnant females. She noticed during pregnancy, when estrogen is at its near high, anagen hairs increased profoundly. At postpartum period (delivery), hair loss soared when estrogen plummeted.[6]

And in this study[7], 20 premenopausal women with pattern hair loss had a lower estradiol:free testosterone ratio.

A healthy liver produces PROGESTERONE, which deactivates estrogens and protects testosterone from converting to DHT. Low progesterone is indicative of hair loss due to more DHT conversion. This is one main reason why postpartum women sometimes lose their hair because progesterone tends to fall steeply.

Then again, female pattern hair loss can also happen in the other direction if there’s too much estrogen and too little testosterone. In vitro (test tube), using female occipital hair follicles and 17-β-estradiol (E2), this study[8] confirms significant inhibition to hair shaft elongation. And in this article[9], estrogen DOMINANCE causes hair loss in women due to thyroid inhibition.

• Unfortunately, there isn’t a gold standard to use, otherwise, hair loss would no longer be pervasive. The best indicator is to watch out for any hormonal DOMINANCE on either side of the estrogen:testosterone scale.
• Like men, the hormonal ratio must be well balanced on both ends. If any one hormone is more DOMINANT than the other, exhaust all options to reach equilibrium.
• Order a blood test for estrogen, free testosterone, and total testosterone to monitor any imbalanced shifts.

Another hormone disturbed by an unhealthy liver is SHBG. An SHBG paucity can lead to diffuse hair loss in some women.[10] It may also contribute to premature androgenetic alopecia (AGA) in men.[11] The theory is by having more SHBG, free testosterone is no longer unbound making it less likely for DHT conversion via 5-alpha reductase.

There are some formidable “forces” one should look out for to keep SHBG stable. If taken lightly, DHT is more likely to invade the hair follicles effortlessly. I’ve labeled them below:

1. Less SHBG = high insulin resistance and glucose in the blood[12] (to read more about insulin, click here for a prologue)
2. Less SHBG = high blood pressure[13] (hypertension)
3. Less SHBG = obesity[14]
4. Less SHBG = higher smaller, denser low density lipoprotein (LDL) or bad cholesterol and increased triglyceride[15]

One of the big stress hormones secreted by your adrenal glands is CORTISOL. Cortisol typically rises in the morning after you get out of bed to prepare you for the day. It then drops in the early afternoon and levels throughout the entire day, unless if there are other stressful inputs (job deadlines to satisfy, relationship problems, etc.). The body releases cortisol during distress (bad stress), when anxiety or fear kicks in as a fight-or-flight mechanism. It can also be produced during eustress (healthy stress), such as when you’re motivated to fulfill a goal.

The type cortisol you should be concerned about is when the body enters into consternation in the form of DISTRESS. When this happens, especially in a repetitious cycle, mitochondrial cellular activity shuts down. In case you’re unaware, mitochondria is the power line that supplies “electricity” to all our cells. If the mitochondria is impaired through continuous stress, it’s unlikely any treatment will have a profound positive effect on hair loss or any other ailment.

Stress can also come in a subtlety, which is overlooked by society. That subtlety is sleep deprivation. Our bodies were made to rest. Even God rested on the seventh day. On average, although age may be a factor, 7-8 hours of sleep per day is the ideal standard to aim for. Chronic, sustained sleep loss, if not taken seriously, ascends cortisol. Even partially losing 3 hours of sleep can radically spike cortisol on the second evening day following the night of sleep.[16] This study[17] further validates the aforementioned finding.

Sleeping less than 7 hours or even 9-10 hours also opens the door for another health “bully” – DIABETES. In a population of 744 participants, the sleep deprivers (< 7 hours of sleep) and the sleep overachievers (9-10 hours of sleep) were directly associated with type 2 diabetes due to higher insulin resistance.[18] Note, if you want to know how INSULIN RESISTANCE is connected to hair loss, click here.

In relation to hair loss, the constant, accrued flow of cortisol blocks TSH from making free (unbound) T4 and T3 from the thyroid to regulate metabolism. T3 is critical for inducing mitochondria. If the thyroid is held “hostage” from the “most wanted public enemy”- CORTISOL– and instead, produces reverse T3, which is inactive, how will you regrow your hair if the mitochondria is suppressed?

TSH is a signal from the pituitary gland to make T4 and doesn’t do anything until it’s converted to T3, which promotes mitochondria and hair growth. If you’re stressed out, you won’t make T4, but instead reverse T3.

Proper mitochondrial signaling using thyroid hormones is vital for instructing the pool of stem cells located in the hair bulge to move and proliferate new hair. When there’s too much cortisol, the liver discharges Thyroid Binding Globulin (TBG). This protein is detrimental because it binds free T4 and T3 in circulation.

When free thyroid hormones are bound, they are inactive. If T3 is no longer free, the cells lose mitochondrial function, progesterone drops, and estrogen elevates. At this point of estrogen dominance, it has been shown TBG directly intensifies[19] creating a perfidious feedback loop, which impairs T3’s liberty.

Because cortisol is “dynamite” to the thyroid, there’s no surprise why balding men and women have immoderate concentrations of cortisol.[20]

PROLACTIN is a hormone secreted by the pituitary gland to stimulate milk production during pregnancy. It’s also produced during physical or emotional stress, similar to cortisol. Too much of it “freezes” the hair follicles in the catagen phase (regression) thereby significantly reducing its size.[21] To further add more color, it may so happen be prolactin only significantly slows anagen entry if it’s abundant and sustained over a long period as demonstrated in this mice study.[22] Temporary prolactin spikes or moderate prolactin levels most likely unalters the hair regrowth cycle unfavorably.

Prolactin also shares a direct affiliation with estrogen and many other molecules, such as prokinetics, opiates, anti-androgens, anti-hypertensive drugs, etc.[23] Until research proves otherwise, estrogen stands out among the list of prolactin-inducers when we think in terms of hair follicle regulation. Estrogen is a prolactin stimuli.[23] If estrogen increases, so will prolactin.[24]

This paper[25] actually does a good job tying the direct connection of estrogen’s, cortisol’s, and prolactin’s response to AGA. All three “silent hair assassin” hormones were elevated in the study, which confirms the strong behavioral correlation they share with each other (e.g. if estrogen increases, that response may very well cause a rise in cortisol and prolactin).

We all know excess estrogen, scarce progesterone, and mitochondrial degradation are one of the major culprits behind a volatile thyroid and with that comes hair deterioration.

Blood sugar control is integral for hair and health survival. Your pancreas manufactures a hormone called insulin. Insulin responds to sugar or any food (refined carbs) that turn into sugar. Its primary job is to reduce sugar in your blood. If you’re hypoglycemic – having abnormally low levels of sugar (glucose) in the blood – the receptors on your cells don’t respond to insulin.

Over time, if insulin cannot enter the cells because the body is not allowing it in a hypoglycemic state, insulin piles up on massive proportions. This can potentially happen if you’re consuming the wrong types of foods mainly a high, refined carbohydrate or sugar diet, which promote excessive fat stored on the liver and pancreas. Lack of sleep and physical inactivity are also common causes.

If the cells are resistant to insulin, sugar will accumulate in the blood over a period of time because insulin cannot enter into the cells to lower the sugar. This is known as INSULIN RESISTANCE, which eventually speeds the onset of DIABETES!

If you’re want a more in-depth explanation on insulin resistance, watch Dr. Eric Berg’s video.[26]

When diabetes comes into play as a result of prolonged insulin resistance, chronic inflammation, and obesity are not only calls for action. What also ends up happening is excessive insulin and glucose in the blood translates into more androgens and less SHBG.[27] For women and men with less SHBG that can mean more free, unbound testosterone is available to convert into DHT. With more DHT floating around your body, depending on your androgen receptors’ sensitivity, the risk of developing AGA can tremendously increase in some, not all cases.

And if that’s still unconvincing, here are three studies cementing the commonality of insulin resistance in AGA:

1. Study #1[28] – also identified diabetes, a derivative of insulin resistance, and high blood pressure (hypertension) in patients with AGA.
2. Study #2[29] – concluded higher insulin resistance in AGA patients emulating polycystic ovary syndrome in women.
3. Study #3[30] – found significant levels of insulin resistance, free testosterone, and lipids in young males with a Norwood type III hair loss.

• Too much or too little sleep elevates cortisol
• Cortisol suppresses thyroid regulation, metabolism, and hence hair growth by blocking the mitochondria and unleashing TBG.
• To miniaturize the production of cortisol, aim for 7-8 hours of sleep daily, exercise, meditate, and eat nutritious, unprocessed, anti-inflammatory foods.
• Excessive prolactin is a stimuli for shutting out the growth of hair follicles.
• Temporary prolactin elevations will probably not block the normal hair cycle.
• Estrogen shares a three pronged relationship with cortisol and prolactin. If estrogen rises, so will cortisol and prolactin.
• Artificial, refined carbohydrates and sugar, over time can lead to insulin resistance by blocking the receptors on your cells for insulin to enter into.
• Insulin resistance speeds the progression of diabetes and androgens and decelerates SHBG.
• With too little SHBG, more testosterone becomes freer increasing the bioavailability of DHT.

Serum (blood) IGF-1 (Insulin Growth Factor) (not scalp tissue) is a growth hormone developed by the liver subsequently when the pituitary gland releases the growth hormone in the blood. It shares a “yinyang” relationship with insulin that gets repleted from the pancreas. That “yinyang” is symbolic of insulin and serum IGF-1 working in unison to determine which type of fuel to use – sugar (insulin) or fat (IGF-1).

The decision rests on whether you consume foods or fast. Eating will cause the pancreas to secrete insulin, thus using sugar. On the contrary, fasting exudes more serum IGF-1, which means more stored fat is recycled as fuel.

Ever noticed why intermittent fasting in the short term is effective for losing weight? Well it’s because serum IGF-1 kicks in as a good side effect from and burns off excess stored fat through fuel consumption. There are other methods of increasing serum IGF-1 like adhering to protein intake, capacious sleep, dairy, grains, and strenuosity.

Due to serum IGF-1 being four to five times more potent than insulin[31] and how various commodities can quickly increase its bodily presence, serum IGF-1 is a highly sensitive wire that can trigger an explosion. The explosion I am referring to is pattern hair loss originating from a hormonal disorder.

Before I get into the serum IGF-1 drama, an important distinction needs to be made between free/unbound and bound serum IGF-1.

What holds more weight when we speak about serum IGF-1 in the context of hair loss is the amount of free vs. bound serum IGF-1. As you will see, research points in the direction that baldness may be caused by elevated free serum IGF-1 and lower insulin-like growth factor binding protein 3 (IGFBP-3). Although that answer is not definitive due to a deficit of follow up studies, the current reports are still present and strong enough to accept this argument. Just like there are current studies validating less SHBG (the binding testosterone hormone) and more free testosterone in bald subjects, it’s in a very similar reason to believe more unbound/free serum IGF-1 can attenuate hair growth.

IGFBP is comprised of a family of six binding proteins. About 98 percent of serum IGF-1 is almost always bound to one of the six binding proteins. I say almost always because if serum IGF-1 is highly elevated, there’s strong reason to believe in respect to the vertex balding study[32], a pronounced presence of free serum IGF-1. If there wasn’t, then those vertex balding subjects would probably have more hair if free serum IGF-1 was bounded to one of the IGFBP family proteins, the most abundant being IGFBP-3.

Note, in that same study, IGFBP-3 was scarce. This type of binding protein is amplified in human dermal papilla hair cells along with IGFBP-5.[33] It also modulates tissue IGF-1 through the production of keratinocytes in the epidermis[34], which play a role in hair follicle formation. And the fact IGFBP-3 influences cellular hair proliferation[35] goes to show it has a significant spotlight in the hair cycle.

Much emphasis should be placed on IGFBP-3 for future hair loss studies given it makes up 80 percent of all IGF binding proteins.[36]

Modest to moderate amounts of serum IGF-1 is not a bad thing. We actually need enough serum IGF-1 for cellular proliferation ranging from muscular and bone growth to brain development to cardiovascular healthiness. It’s when we have a surfeit where danger is at close waters. Unfortunately, because of my ignorance, I became that victim of overloading on serum IGF-1 through WHEY PROTEIN SHAKES, which costed me most of my hair.

Before we take an excursion to my ominous whey protein story, allow me to quickly switch gears to the relevance of TISSUE IGF-1. Tissue IGF-1 is not the same as serum IGF-1. The former actually regrows hair by attaching to the IGF-1 receptors on the scalp thereby regulating the hair cycle. As indicated in this mice study, exogenous application actually prolonged the anagen phase and regrew hair on bald mice.[37] It’s a potential strong hormone to accelerate hair growth that Japan’s famous director, Dr. Kenji Okajima, and his research team have founded an IGF-1 treatment clinic.[38] Tissue IGF-1 is also induced in the scalp by wounding (e.g. dermarolling) or other mechanical stress techniques (e.g. massaging or bristle boar brushing).

So, the big takeaway is serum IGF-1 only in prodigious amounts is deadly to the hair whereas tissue IGF-1 is pro-hair.

Circling back to my horrific whey protein story, at age 22 I was taking a ridiculous amount of four scoops per day five days a week to gain muscle mass. To give you some perspective on how many daily grams of protein that was exclusive from my normal dietary meals, 96 grams was the lucky number!

Now, take that number and add it with the 60 or so grams of protein I got from my inflammatory diet each day. And it doesn’t end there! Add on weight lifting plus cardio exercises four days a week along with 8-9 hours of sleep per day for a two year time span. Can you guess what kind of impact my rigorous regimen had on my liver? A constant, colossal overflow of serum IGF-1. And because my liver couldn’t handle all the protein, especially the artificial whey kind, more insulin was also unleashed according to Dr. Berg.[39]

I think the science will be a lot clearer if I rewind and take a snapshot of my observations in the past to see how they line up with the medical literature.

Regular intake of inflammatory, refined carbohydrate, and refined sugary foods (grains, polyunsaturated fats, etc.) raised my insulin to lower the high glucose from these high glycemic foods. My liver also produced more free/bioavailable (unbound) serum IGF-1 in response to this high glycemic load diet.

As indicated in this study, it’s known a Western diet both increases insulin and IGF-1, which overtime, can lead to other complications like type 2 diabetes and cancer.[40] Hyperestrogenemia (excess estrogen) is also heavily influenced by such a diet[41] shifting the estrogen:testosterone ratio to one that’s more estrogen dominant. With more insulin, estrogen, and free serum IGF-1 cruising in my blood stream, my body and hair were in for a big, grisly surprise.

Probably, the only good aspect about my Western diet was that it was modified to the extent of eating organic meats (cold cuts, chicken, and turkey), milk, some grains (white rice), and wild caught seafood. If we were to extrapolate the most nutrient-dense foods, chicken, turkey, and seafood would be the winners.

Even though, I was eating a modified Western diet, my diet was still not pristine. I ate other low-quality foods particularly cold cuts, dairy, and whey protein. Despite cold cuts and milk being organic, their biological content still made them risky in terms of insulin-dependency as these medical studies point out:

1. Processed meats increases the risk of type 2 diabetes, a symptom of insulin resistance6[42]
2. Milk and fermented dairy like whey protein are higher insulinemic foods[40]
3. Milk consumption based on 3 servings raises free serum IGF-1 by 18.6 percent[43]

When it comes to whey protein shakes, it was a beast of its own as my next observation reveals.

I am doubly and highly convinced my overdose on whey protein shakes was the deal breaker for ruining my health and hair. Here are a mixture of eight plausible theories, observations, and factual evidence proving why I am against whey protein/high-protein diets and how it directly lead to my pattern baldness: