Is there really a smarter way to stop hair loss? An approach that does not involve playing around with the androgens, testosterone and its more powerful metabolite? What if there was a way to maximize muscle size, strength, libido, mood and keep your hair at the same time? There is indeed a way to stop this hair miniaturization madness without having to resort to petrochemicals that throw your endocrine system into a loop!
Why Testosterone & DHT are Not your Enemy
Before we delve into this topic, let’s understand first and foremost that testosterone and dihydrotestosterone (DHT) are not the enemy. Before you stop reading, consider for a moment that when testosterone is bound to sex hormone binding globulin (SHBG), it cannot be converted into DHT via the enzyme 5-alpha reductase.
In other words, only free testosterone (unbound) is subject to conversion to DHT by 5-alpha reductase. Research has shown that when hormone parameters are measured in balding vs non-balding men, there is a significant reduction in SHBG levels observed in bald men, compared with non-balding. 
Balding Men Typically Have Lower Testosterone & DHT levels
Originally published in 1992, the American Journal of Physical Anthropology examined total testosterone and DHT in blood serum as well as free testosterone in saliva in 110 healthy young men. The absolute serum androgen concentrations in men with a disposition to balding is lower than in men with no alopecia (hair loss).
The popular assumption (myth) that androgen levels are generally elevated in balding men should be rejected. In accordance with this finding, men with a disposition to balding are morphologically no more masculine than those with good scalp hair growth. When body build and age are taken into consideration.
Simply stated, non-balding scalps typically have higher serum (blood) levels of DHT. This is not a misprint. 
How Does the Enzyme 5-AR (5-alpha reductase) Fit into this Equation?
Let’s get one thing about of the way first as you might be wondering how the enzyme 5-alpha reductase fits into hair loss. The answer is, yes it does matter. In fact, androgenetic alopecia or hormone mediated hair loss is absolutely correlated with this enzyme. Note that while serum (blood levels) of DHT are inversely correlated with hair loss, salivary DHT is directly correlated.
So to be clear, if you test your serum DHT level, it’s not going to be of any real value. Generally speaking, young men who bald have low levels of SHBG, which allows plenty of unbound testosterone to freely convert via 5-alpha reductase. However, as we age, our SHBG levels naturally increase. As we approach middle-age, these are often too high and we may suffer from a lack of bio-available testosterone. Also with respect to aging, through the process of aromatization (conversion of testosterone into estrogen) as well as increased production of 5-alpha reductase, local tissue expression of these enzymes affects hair and androgen levels alike. 
What’s the Real Culprit in Male Pattern Baldness (MPB)?
The simple explanation is inflammation. Inflammation is not always obvious, it can produce a low-grade chronic infection that is not always visible to the eye. Inflammation involves a form of oxygen deprivation, which in the case of hair loss can result from an infection.
When androgens are affecting local tissue, the difference between a balding and non-balding person is that significantly more DHT is necessary to inflame the latter. However, those who bald are quite sensitive to DHT, and a result generate a high volume of reactive oxygen species (ROS). Think of ROS as free-radicals.
Reactive oxygen species are associated with accelerated aging in cells (senescence). Moreover, ROS by way of oxidative stress (free-radicals) damages cellular DNA, proteins and fatty acids. If that sounds bad, well it is, and as a result induces transforming growth factor-beta (TGF-β) in hair producing cells called the dermal papilla.  It is transforming growth factor-beta that stops the growth of hair follicles. Simply stated, TGF-β is a hair follicle assassin. If it can be tamed, your hair can take less of a “hit” without having to experiment with hormones.
Neutralizing the ROS Effect
When physiological levels of androgen exposure exist to boost reactive oxygen species (ROS) generation in androgen “sensitive” hair follicles, TGF-β1 secretion can be mitigated. How? The very best way is to boost your body’s ability to increase its own antioxidant enzymes. These antioxidant enzymes, such as superoxide dismutase (SOD), glutathione peroxidase, and catalase all work together in human cells against toxic reactive oxygen species.  Reactive oxygen species (ROS) are not always bad, they have a purpose. Low concentrations of ROS can be beneficial or even indispensable in processes such as intracellular signaling and defense against micro-organisms. Standard antioxidants are not nearly sufficient to halt the process because they do not generate antioxidant enzymes. However, antioxidant enzyme boosters can. Certain plant and sea-based polyphenols can epigenetically “turn on” gene and/or transcription factors that will boost the level of antioxidant protection within inflamed tissue. These are thousands of times more powerful than the traditional antioxidants.
So let’s review…androgens are involved in ROS generation, and ROS is related to TGF-β secretion. This is one of the significant events that are involved in androgenetic alopecia or male pattern baldness. In tests during sub-cultivation of hair cells (dermal papilla cells), sensitivity to androgens may be low because of the reduced expression level of the andogen receptor. Androgen receptors are expressed at higher levels within the hair cells of bald frontal scalps than those of non-balding occipital scalps.
The most effect antioxidant enzyme boosters for hair growth purposes in my experience are the following: Ecklonia cava, curcumin, and trans-resveratrol.
. American Journal of Physical Anthropology Volume 88, Issue 1, pages 59–67, May 1992
. Arch Dermatol 1986;122:1011-1015
. BMB Rep. 2013; 46(9): 460-464
. J. Endocrinol. 156, 59-65.