Goal: Hormone balance
Approach: Optimize thyroid, estrogen, testosterone, progesterone, pregnenolone, and cortisol with the help of your doctor
Thyroid function affects metabolic speed (hot/cold, over- versus under-weight), heart rate, mental sharpness, and mood. Here are the optimal levels:
- TSH < 2.0 microIU/ml
- free T3 = 3.2-4.2 pg/ml
- reverse T3 < 20 ng/dL
- free T3 X 100:reverse T3 > 20
- free T4 – 1.3-1.8 ng/dL
The role of estrogen and progesterone in women is not totally settled, but within the brain, estrogen regulates the production of energy, use of glucose, and mitochondrial function. We know that women are at higher risk for AD, and during menopause, the decline in circulating estrogen coincides with cognitive impacts and brain energy deficits. Dr. Bredesen suggests the following levels for women:
- estradiol = 50-250 pg/ml
- progesterone = 1-20 ng/ml
- estradiol:progesterone ratio = 10:100 (and optimize to symptoms)
T (Testosterone) is the primary male sex hormone. Attention, memory, and spatial ability are affected by testosterone, and low or high testosterone levels may be a risk factor for cognitive decline and possibly Alzheimer's. Dr. Bredesen suggests the following levels for men:
- total testosterone = 500-1000 ngo /dL
- free testosterone = 6.5-15 ng/dL
Pregnenolone is a steroid hormone. It is the precursor of many other steroid hormones and acts as a neurosteroid itself.
Cortisol is a stress hormone. Long-term exposure to cortisol damages cells in the hippocampus and impairs learning. Cortisol also decreases memory retrieval of already stored information.
Scientists don't know everything DHEA does. But they do know that it functions as a precursor to male and female sex hormones, including testosterone and estrogen.
Dr. Bredesen suggests the following levels:
- cortisol (morning) = 10-18 mcg/dL
- pregnenolone = 50-100 ng/dL
- DHEA sulfate (women) = 350-430 mcg/dL
- DHEA sulfate (men) = 400-500 mcg/dL
- Next generation therapeutics for Alzheimer's disease
- Estrogen use, APOE, and cognitive decline: evidence of gene-environment interaction
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