All you need to know about LH and the LH to testosterone ratio

How it works

Kisspeptin and NPY promote the release of GnRH in the hypothalamus. GnRH stimulates the pituitary to release luteinizing hormone (LH) and follicle-stimulating hormone FSH.

LH stimulates the Leydig cells in the testes to produce testosterone (enhance uptake of cholesterol and conversion in pregnenolone, etc.) and FSH stimulates the Sertoli cells to produce sperm.

As you can see, there are many places where things can go wrong, namely inhibition at the hypothalamus, pituitary and/or testes.

Different kinds of LH to testosterone ratios

The LH to testosterone ratio can tell you a lot about where the issue is coming from and what you can do about it.

We’re going to look at:

  • Normal LH, normal T
  • High LH, normal T
  • Low LH, normal T
  • High LH, low T
  • Normal LH, low LH
  • Low LH, low T

Normal LH, normal T

It’s important to start with what’s normal and what to shoot for.

A good LH range is typically 4-8, but this depends on where you’re other hormones, inflammation, blood sugar control, and gut health as well.

A good range for testosterone depends on how sensitive someone is to the testosterone. They might get away with 300ng/dl, whereas someone else will feel best at 1200ng/dl. However, if things aren’t in order, even >1000ng/dl won’t be enough.

Check out this video where I discuss testosterone ranges.

The LH level is mostly determined by Leydig cell function, inflammation, infection, and other hormones (estrogen, prolactin, etc.). We’ll get into that in a bit.

LH, testosterone and normal aging

Is it possible to have normal LH and testosterone into old age?

Yes definitely. Previous studies showed that testosterone dropped by 1-2% per year after the ages of 30-40. Diseases cause this to drop even faster. This gives you the idea that low testosterone is inevitable.

However, accumulating evidence from newer studies suggest that age-related fall in serum total T is closer to 0.5% per year (R).

Additionally:

We show that total testosterone peaks [mean (2.5–97.5 percentile)] at 15.4 (7.2–31.1) nmol/L at an average age of 19 years, and falls in the average case [mean (2.5–97.5 percentile)] to 13.0 (6.6–25.3) nmol/L by age 40 years, but we find no evidence for a further fall in mean total testosterone with increasing age through to old age.” (R)

Hypogonadism isn’t inevitable, as long as you look after yourself.

In another study, no appreciable change in serum testosterone up to the 8th decade of life was observed among men with self-reported very good to excellent health (R).

In European Male Aging Study (EMAS), 2,736 men aged ≥40 years were followed up for an average of 4.4 years, and >80% of men in their 7–8th decade continued to have normal T values (R).

Therefore, LOH (late onset hypogonadism) is less prevalent than previously thought, and low T in older men is mostly related to co-existing medical conditions and obesity.” (R)

What really causes low testosterone? Not looking after yourself.

The majority of older men were found to have low T associated with low-normal luteinizing hormone. This is not independently associated with aging per se but is mediated indirectly via age-related non-gonadal co-morbidities, including obesity, and increased visceral adiposity. Only a small number of older men (2.1%) had low T with high LH, in keeping with primary testicular insufficiency. This specific primary hypogonadism profile has been directly associated with both aging and metrics of ill health.” (R)

High LH, normal T

In hypogonadism, there are 3 main categories:

  • Primary hypogonadism (LH >9.4 u/L, T <10.5 nmol/L) (high LH and low T), or
  • Secondary hypogonadism (LH ≤9.4 u/L, T <10.5 nmol/L) (low LH and T), or
  • Compensated (primary) hypogonadism (high LH, normal T)

High LH and normal T aren’t that common, but it can happen and it’s called compensated hypogonadism, if the measures are LH >9.4 u/L (range 1.42 to 15.4 IU/L), T ≥10.5 nmol/L (>300ng/dl).

Elevated LH in the presence of low or normal testosterone is a problem in itself.

There are LH receptors everywhere in the body, not just in the Leydig cells. Chronically elevated LH (even with normal T) has been associated with both decreased muscle strength and increased cardiovascular disease risk factors (high blood pressure, fasting blood sugar, cholesterol, triglycerides and hsCRP) and ~10-fold increased risk of cardiovascular mortality regardless of where testosterone levels were.

LH is an independent predictor of impaired endothelium function and morphology, which can play a role in atherosclerosis, similar to excess TSH in subclinical hypothyroidism.

LH stimulates aromatase, which enhances the conversion of testosterone to estradiol, and a higher E-to-T ratio is also undesirable for many reasons.

Lastly, high LH with normal/high testosterone can also be caused by hyperthyroidism. Hyperthyroidism enhances LH release to GnRH, leading to high LH, normal/high T, E and SHBG (R). Often enhanced LH/FSH ratio as well.

Low LH, normal T

Low LH, according to me, is below 4. And low LH with normal T, 800+, is also not that common. It mainly indicates that your testes are very sensitive to LH and that there aren’t many things inhibiting the testes. However, there might still be things that lower LH.

We’ll discuss that in the “low LH, low T section”.

Alternatively, someone is using HCG, which lowers LH and increases testosterone.

Interestingly, LH plasma levels were significantly higher in patients with hypersexual disorder than in healthy volunteers. No significant differences in plasma testosterone, follicle-stimulating hormone, prolactin, and SHBG levels were found between the groups (R).

High LH, low T

This is called primary hypogonadism, which is caused by testicular dysfunction. The pituitary is likely working just fine and pumping out more LH to stimulate the testes.

High LH is a biomarker for deteriorating health in aged men who tend to develop primary hypogonadism (R).

What causes high LH

  • Oxidative stress – 4-hydroxynonenal (4-HNE), a sensitive marker for oxidative damage, increased with age and leads to an increase in LH and LH/T ratio (R).
  • Testicular dysfunction – a recent study has demonstrated that healthy older men without late-onset hypogonadism (LOH) have preserved hypothalamic response to kisspeptin-54 and pituitary response to GnRH, with an impaired testicular response as compared to younger men (R). This suggests that primary testicular failure accounts principally for the normal aging-related decline in T production. In the majority of healthy older men, the compensatory increase in gonadotrophins serves to maintain T levels within eugonadal ranges.
  • Microplastics – These cause testicular insensitivity (R).
  • Liver disease – This leads to low T, high LH and FSH and high estradiol (R). Mild fatty liver will have a mild effect and the effect will get stronger the worse off the liver is.
  • Amiodarone, an antiarrhythmic drug, causes testicular dysfunction which causes very high LH and FSH (R).
  • Angiotensin II. Angiotensin II is produced by ACE. ACE overexpression increases LH, but can lower testosterone since angiotensin II is inflammatory and causes vasoconstriction (R, R). Zinc is used by ACE and ACE2, which create and deactivates angiotensin II.
  • Vitamin E deficiency – Low vit E leads to higher LH, desensitized LH receptors and lower T and enhances oxidative stress and inflammation (R, R, R).

Smoking lowers vitamin E and causes oxidative stress and smokers have higher LH and lower T than non-smokers (R).

Normal LH, low T

This is usually due to testicular failure as well. Also in some cases, something can lower both LH as well as cause testicular failure and this might cause a compensatory increase in LH, making it appear to be normal.

Things that can cause low T without affecting LH:

  • Low fat diets reduce testosterone without affecting LH much (R).
  • Selenium can help to increase testosterone but doesn’t seem to have a direct effect on LH. It might have an indirect effect by increasing glutathione, thus protecting the testes.
  • Magnesium improves ATP levels and lowers oxidative stress and inflammation, which will help to increase testosterone and the T to LH ratio.
  • Vitamin D increases testosterone and the testosterone to estrogen ratio as well as the testosterone to LH ratio (R). There are also many studies showing that vitamin D doesn’t increase testosterone, but that vitamin D levels are associated with testosterone. So it’s moreso sunlight that increases testosterone, and not so much the vitamin D that’s having the majority of the benefits. Rather the minority.
  • Vitamin A – A vitamin A deficiency can slightly lower LH, but decreases testosterone more, which increases the LH/testosterone ratios, suggesting Leydig cell hyporesponsiveness in vitamin A deficient animals (R, R). The cytological changes in the pituitary gland and the increased discharge of FSH represent a secondary and compensatory change similar to that seen following castration and vitamin E deficiency.
  • Low vitamin B5 – Low testosterone (but not LH) in B5 deficient animals (R).
  • Low vitamin B6 – Vitamin B6 deficient animals have either a reduced rate of synthesis of testosterone or an increased rate of metabolic clearance compared with vitamin B6 supplemented controls, but normal LH (R).
  • Estrogen – Estrogen lowers LH and decreases LH responsiveness in the testes (R), but it also damages the testes, which could cause a compensatory increase in LH, thus making LH seem normal (R).
  • (Very) high SHBG which prevents the negative feedback loop.
  • Endotoxin. Endotoxin is produced by bacteria in the gut and when you have SIBO or leaky gut (caused by gut inflammation or stress), endotoxin enters the body. Even a low small amount of endotoxin (produced by pathogenic E. coli) in lean men produced a transient inflammatory response that was followed by a decline in serum testosterone, without changes in LH or FSH, providing further evidence that endotoxin-driven inflammation may result in impaired Leydig cell function (R).

Low LH, low T

Secondary hypogonadism accounted for the majority (85.5%) of older men with low T (R).

What causes low LH

  • Diabetes – “Pituitary sensitivity to exogenous GnRH has also been observed to be reduced by 67% (P=0.001) in castrate rats with diabetes.” (R)
  • Obesity – Individuals with BMI ≥30 kg/m2 are at 13-fold increased risk of LOH compared to those with BMI <25 kg/m2 (R). Fat tissue, especially visceral fat, expresses more aromatase and releases more inflammatory mediators and leptin (which causes leptin resistance), all of which lower testosterone (R).
  • Prolactin – High prolactin and a high prolactin-to-testosterone ratio is the best independent predictor of finding a pituitary abnormality on magnetic resonance imaging, leading to low LH to FSH ratio (R).
    • After three weeks, the prolactin level had fallen and the gonadotropin levels had shown a substantial rise, reaching supraphysiologic levels by eight weeks, eventually returning to normal by 15 weeks. The serum testosterone level did not rise until after three weeks and reached a maximum by 15 weeks. When the bromocriptine therapy was stopped for one week, all indexes returned to near pretreatment levels. Within two weeks of re-treatment with bromocriptine, the prolactin level had fallen and both testosterone and gonadotropin levels rose. These findings suggest that prolactin may block the secretion of luteinizing-releasing hormone, or may prevent the pituitary gland from responding to it.” (R)
  • Iron overload (R, R) – Iron loves to accumulate in the pituitary, mostly in the gonadotrope cells, which leads to fibrosis and low LH. Giving blood can reverse it depending on the severity of the condition ofc.
    • MRI studies demonstrate increasing iron deposition and decreasing pituitary volume as body iron stores increase [1112]. Pituitary iron levels are negatively correlated with serum testosterone levels [11]… In the United States, the average male consumes 10–15 times more iron than needed to replenish incidental losses… These data indicate that iron can have toxic effects impacting pituitary function in the general population.” (R)
  • Traumatic brain injury (R).
  • Autoimmune conditions and inflammatory diseases (R).
  • A tumor (R) – The most common etiology is a sellar or suprasellar lesion, often an adenoma, which causes hypopituitarism due to tumor mass effects, or the effects of surgery and/or radiation therapy.
  • Low leptin or leptin resistance, such as in diabetes and obesity – leptin activates kisspeptin neurons to stimulate GnRH, and leptin deficiency/resistance is associated with hypogonadotropic hypogonadism (R).
  • Estrogen – SERMs with antiestrogenic effects in the CNS as well as aromatase inhibitors increase circulating LH as well as testosterone levels in normal men. Men with low aromatase expression or aromatase deficiency often have high LH and testosterone levels (R). 
  • Excess DHT – Blocking 5-AR can increase testosterone a bit, but it will often make you feel less androgenic. This is because DHT is the most potent androgen and most of the effects of testosterone are via DHT.
    • DHT inhibits GnRH release at the hypothalamus, unlike estrogen which inhibits LH release at the pituitary.
    • This study found that exogenous DHT doesn’t suppress LH, but does lower testosterone and SHBG (R). High levels of plasma DHT (induced by exogenous DHT), maintained over a long period (3 months), were unable to lower plasma LH in either normal or hypogonadal patients.
    • Having your DHT naturally high might actually increase testosterone. DHT inhibits the aromatase and doesn’t lower LH in response to GnRH (R).
  • Hypothyroidism – This causes low LH, LH receptor numbers, testosterone, SHBG and free T with a high E to T ratio as well as slightly elevated prolactin (R, R, R, R, R, R). There are T3 receptors in the testes as T3 is very important for testosterone production.
    • TSH regulates testicular function and progesterone and testosterone production. Normal T4 and T3, but high TSH, can reduce testosterone (R).
  • COVID and/or long COVID – COVID-19 causes hypothalamus and testicular dysfunction (low GnRH thus low LH, testes being unresponsive to LH, testicular atrophy and drop in spermatogenesis) (R).
  • Stress.
    • Cortisol. Cortisol is released by stress, which lowers LH and inhibits LH-induced T synthesis (R). Low cortisol can lead to low LH release, whereas high cortisol inhibits its release. Prolactin is also elevated with low cortisol and high cortisol. The suppressive effect is likely that cortisol promotes the release of opioids than suppress LH (R).
    • Catecholamines (adrenaline and noradrenaline) – Interestingly dominant animals experienced an increase in T from stress, whereas subordinate animals experience a drop in T (R). This suggests that sympathetic catecholamines, released during stress and acting peripherally, directly, or permissively lead to increased T concentrations. This could be via increased blood flow through the testes and/or through direct stimulation of T release by catecholamines.
      • Chronic elevations in catecholamines lower T. Beta-agonists reduce LH increase to GnRH (R), whereas beta-blockers can increase LH.
    • Opioids. Opioids are released by stress, which suppresses pituitary function and LH release (R). Dietary opioids, such as gluten and A1 casein can have the same effect. This study found that wheat germ agglutinin (a lectin in wheat)-inhibition of LH release stimulated by GnRH was dose-dependent (R).
  • Low copper – Copper enhances LH release to GnRH (R) and enhances steroidogenic enzymes in the testes (R), whereas an excess might lower testosterone. This study found higher levels of copper and elevated Cu/Zn ratio in hair tissue are associated with lower serum testosterone (R).
  • Arsenic lowers LH and testicular function and has very similar effects to estrogen (R, R). Arsenic also decreases dopamine and increases noradrenaline and serotonin in the hypothalamus and pituitary which lowers LH. 
  • Lead toxicity – Lead accumulation can cause pituitary and testicular dysfunction and cause low LH and T (R).
  • Mercury (R) – There is a significant, inverse relationship between chronic mercury exposure and levels of luteinizing hormone (LH).
  • Cadmium toxicity (R, R) – Cadmium accumulates in the pituitary where it lowers LH release and promotes prolactin release (R).
    • Mimosa pudica (29mg/kg) prevents cadmium induced prolactin increase.
    • Selenium, carnitine and CoQ10 (and Chaste tree (R)) are synergistically protective against cadmium-induced testicular toxicity (R, R).
  • Low zinc – Zinc increased LH and testosterone in male patients on hemodialysis (R), whereas zinc-deficient rats had high LH and low T (R). Zinc supplementation of marginally zinc-deficient normal elderly men for six months resulted in an increase in serum testosterone from 240ng/dl to 460ng/dl in 6 months (R).
    • Zinc is used by ACE2, which deactivates angiotensin II, which lowers T (R, R).
  • Elevated homocysteine – Higher homocysteine is inversely associated with lower LH (R).
  • Hypoglycemia (R).
  • Dehydration – dehydration (and hypoglycemia) increases arginine vasopressin (AVP) and prolactin, which lowers LH (R).
  • Drugs, such as anti-psychotics (due to less dopamine and more prolactin), SSRIs, glucocorticoids, opioids (morphine, codeine, fentanyl, Tramadol, etc.), etc, lower LH.
  • Endotoxin – Above I mentioned that a bolus of endotoxin lowers T, but not LH, however, that’s just acutely. Chronic exposure to endotoxin lowers LH as well, and blocking the endotoxin receptor, TLR4, prevented this (R).
  • Inflammation – IL-1beta is the most potent pro-inflammatory mediator to lower GnRH and LH (R). Inflammation can come from a lot of places, such as heavy metals, gut issues, stress, sleep loss, inflammatory foods, etc.
  • Low manganese – manganese increases dopamine, GnRH and subsequently LH (R), whereas excessive manganese increases GABA, which lowers LH (R). This might happen from excessive intake of fortified plant foods or from inhalation.
    • In excess, it can reduce testosterone synthesis by being directly toxic to the testes (R).
    • The accumulation of manganese in the basal ganglia produces an irreversible neurological syndrome similar to Parkinson’s disease.
  • Environmental pollutants, such as pesticides, radiation, air pollutants, agents originating from plastics, and other endocrine disruptors, are important contributing determinants of hypogonadism (R).

Summary

Hypogonadism isn’t inevitable as long as you look after yourself.

Three things are most important:

  • Eat a nutrient-dense diet
  • Avoid illnesses, with dietary and lifestyle protocols/habits.
  • Avoid heavy metals, drugs, and environmental toxins (plastics, pesticides, etc.)

Contact me to find the root of your low testosterone, by reaching out or scheduling a free call here.

Learn how you can double, triple and in some cases even quadruple your testosterone!

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