low libido/ED, looking for answers

[wondering]

Dr. Mariano – thank you for your wonderful forum.

I am 42 and have suffered from low libido and ED for over 10 years, all the way back into my 20s. I am a difficult case for all my doctors. I take Testosterone, Armour +Levothyroxine, 10mg HC, TD Pregnenolone, DHEA.

If my recollection is correct, you have stated that low SHBG is usually the result of:
1. insulin resistance
2. high levels of exogenous androgens (testosterone)
3. hypothyroidism

My SHBG has always been low and it appears the above are NOT an issue for me. Labs from last summer and a month ago

LABWORK 6/11/11
– SHBG 20 (11-80)
– Testosterone 628 (300-890)
– Fasting Glucose 91 (65-100)
– Free T4 and Free T3 at top of range, TSH under 1.0
– Estradiol is in check

LABWORK 8/2/12
– SHBG 18.9 (17.3-65.8)
– Testosterone 360 (300-100) I changed method of delivery and am in the process of increasing dose per this result.

I also have had recent bouts with Shingles. I’m young for this??

I have often wondered about Anemia and perhaps my body wasn’t using the Thyroid that was available. And the MCV and MCH results below increase my wonder. My PCP wasn’t concerned as I am 100% Greek and figured it was a result of Thallesmia minor (the not so bad kind). Plus my Ferritin was in 90s (I understand you like it closer to 150)

Curious your opinion.

WBC 6.6 (4.0-11.0)
RBC 5.89 (4.40-6.20)
HGB 14.0 (13.0 – 18.0)
HCT 42 (40-52)
MCV 71 (80-100)
MCH 23.8 (26.0-34.0)
MCHC 33.5 (32.0 37.5)
RDW 14.1 (0.0-15.2)

Ferritin – 95

thank you.

[DrMariano2]

Outside of structural damage to the peripheral nerves and circulation that closely serve the reproductive organs such as what may occur with diabetes neuropathy and vascular disease, libido and erectile dysfunction are brain problems.

Within the brain, are specific circuits that need to be active for libido (and erectile function). Some circuits involved include:

• the libido circuit (amygdala, the bed nucleus of stria terminalis, the hypothalamus preoptic are and ventromedial nucleus, the periaqueductal gray),
• the seek circuit (nucleus accumbens to ventral temental area, hypothalamus medical and perifornical zones) to periaqueductal gray),
• the care circuit (anterior cingulat, bed nucleus of straia terminalis, preoptic hypothalamus, ventral tegmental area, periaqueductal gray), and
• the joy circuit (diencephalon, parafascicular area, periaqueductal gray).

In addition, other circuits which can negate libido need to be suppressed. These include the anger, fear, and panic circuits.

Additionally, the sensory-motor strip which processes the sensory information from the reproductive organs and other erogenous zones needs to be an active and metabolically robust group of brain cells – otherwise the mental representation and sensitivity of the organs and erogenous zones will be reduced. Memory circuits and motor circuits are also recruited to process and store information about sex.

This is where the lack of sexual activity or masturbation can be destructive since number of brain cells devoted to sex diminishes. The brain’s representation of the penis shrinks without use. With age and programmed death of cells that aren’t used, the number of cells devoted to sex diminishes.

The brain is a use it or lose it system. This is one way men feel their penises are shrinking and become insensitive when they stop engaging in sex, when the penis remains physically the same size when erect. Practice is necessary to maintain libido, even when one doesn’t have a libido. Penis exercises may need to be done if one doesn’t have libido in addition to optimizing physiology in order to improve the number and activity of cells devoted to sexual function.

There are numerous signals that can turn on the libido circuit, not just testosterone. There are numerous signals that turn off the libido circuit. Each of the main circuits has numerous signals that turn them on and turn them off. The circuits also need to have adequate nutrition and energy production to function.

Thus if testosterone, estrogens, thyroid hormone, and DHEA are already optimized, and if problems with libido are still present, then problems are occurring in other areas.

Some of the signals affecting the libido-related circuits include:
• ACTH
• aldosterone
• cholecystokinin
• cortisol
• corticosterone
• CRH
• DHEA
• dihydrotestosterone
• dopamine
• estrogens
• GABA
• glutamate
• growth hormone
• leutenizing hormone-releasing hormone
• melanocyte stimulating hormone
• neurotensin
• norepinephrine
• endogenous opioids
• oxytocin
• pro-inflammatory cytokines (e.g. IL-1b, IL-6, Tumor necrosis factor, etc.)
• progesterone
• prolactin
• serotonin
• testosterone
• thyroid hormone
• vasopressin

Note that hypothalamic-adrenal dysregulation is a brain problem, not an adrenal problem in nearly all patients. My preference is to address the brain problems as directly as possible. Adding exogenous cortisol can be a problem since it shuts down production of many signals that have a positive effect on the libido-related circuits, including ACTH, progesterone, corticosterone, MSH, endogenous opioids, etc.

Nutrition has to be optimized. Without adequate iron, for example, dopamine can’t be produced. Assessing iron metaboism not only needs Ferritin, but also serum Iron, CBC, Vitamin A, Copper, etc. etc.

SHBG is a small player (which also means free Testosterone is a small player). There are more important considerations. It’s level is determined by more than 6 different hormones which can go in opposite directions. Insulin, is the strongest signal and it suppresses SHBG production. Outside of insulin and over-physiologic levels of testosterone, what level of SHBG one has doesn’t tell much about what problems there are with the hormones that influence it. A normal SHBG doesn’t tell if there are problems with these hormones since the problems can negate each other’s effect on SHBG. Once excessive insulin signaling is addressed and total testosterone is optimized, my preference is to look for more important problems than SHBG issues when it comes to libido.

[wondering]

Thank you for your detailed response.

While I am not a doctor, I do have the advantage of living with my body every moment of my life. By reading information from yourself and Dr. Crisler over the past years, I pay very close attention to how I feel and comapre ot what I have learned.

I have become increasingly convinced, I have an overactive Sympathetic Nervous System, cause of which I am not sure. I often see you post abpu the effects of too much norepiniphrine and how it can inhibit erections and libido. Need it, but not too much.

Even though my last Testosterone blood test showed only 360, a 24h urine test done at the same time ,showed DHT above range. I believe I read once that Dr. J stated that sometimes, it seems androgens can all be driven to DHT and can “burn up the circuits” so so to speak.

How do you feel about such a scenario?

What causes excessive DHT? How to combat without risking Finasteride?

Progesterone counters?

I have used a Mindful practice to help calm myself down, but this doesnt seem to be enough.

thank you again.

[wondering]

As stated, I have become convinced I have excessive norepiniphrine. I have poor libido, ED and PE. I can orgasm with ease, mutiple times in hours, but always with very poor erections and lack of feeling. Just kinda happens.

To complete my iron labs:

Iron 52 (45-170)
TIBC 287 (250-450)
Transferrin Saturation 18 (20-55)
UIBC 235 (110-370)
Ferritin 96 (20-250)

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