Nutrition and hormones: how blood sugar also moves estrogen and cortisol
Blood sugar does not reach into your hormone system in some vague way. It does so through four namable places, and three of them lie not in ovary or testis, but in liver, fat tissue and gut.
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Almost everything written about nutrition and hormones ends in one sentence: eat less sugar and your system will settle. That sentence is not wrong. It is just too coarse to explain anything to you. Between the bite and the messenger molecule sit four well described translation points. And the largest study on the topic is not about the peak, it is about the dip that follows.
It is half past three in the afternoon. You had lunch, a decent one. And still you sit there: slightly shaky, thin skinned, and your head thinks of nothing but something sweet. Many people know this. It feels like weak willpower. What sits behind it is often mostly biochemistry.
Later you read somewhere that sugar throws your hormones off. And you think: fine, but what does that mean for me?
That is exactly where I want to go with you. Blood sugar is one of the fastest levers nutrition has on your hormone system. Not because sugar is a poison, but because insulin and cortisol work on the same axes as your sex hormones.
What you will find here
- SHBG in the liver as the first translation point
- What insulin can set off in the ovary in PCOS
- Why aromatase in fat tissue matters for men
- The four thresholds at which cortisol steps in
- Why the dip says more than the peak
- How cortisol, belly fat and insulin close a loop
- Estrobolome, fiber and the conflicting data
- When too little energy becomes hormonally expensive
- Twelve questions from my consultations
Why your hormone panel can depend on breakfast
You may know this: two hormone panels, eight weeks apart, and the numbers look like they came from two different people. You did nothing differently. At least nothing you noticed.
Hormones are not a still image, they are a course over time. One of the fastest pacemakers within it is blood sugar. It is not a hormone itself, more the conductor several sections of the orchestra follow.
Conventional nutritional medicine looks at calories, macronutrients and weight here. That is sensible and important. What an integrative view can add are the steps in between: the places where a metabolic signal is translated into a hormone signal.
Liver
Insulin and lipogenesis throttle SHBG, more free hormone becomes available.
Stress axis
The dip after the peak calls in adrenaline, glucagon and cortisol.
Liver and gut
Estrogen is conjugated, excreted, and partly reactivated by gut bacteria.
Energy brake
Too little energy dampens the pacemakers in the brain.
The common question is: which food throws my hormones off? A more useful one is: at which of the four translation points am I standing right now?
The same way of eating can land in different places in two people. In one at the ovary, in another in fat tissue, in a third in the gut.
And that makes it clear why a hormone value is always a nutrition value too.
Chain one: the liver decides how much hormone is free at all
Imagine a panel: testosterone within range, estradiol within range, nothing unusual. And still something is off. I see this very often in my consultations.
Often it comes down to a protein hardly anyone knows: SHBG, sex hormone binding globulin. It is built in the liver and carries testosterone and estradiol. Picture a doorman. Whatever he holds on to cannot dock. When SHBG falls, the free share of both hormones rises, even though the total values can stay the same.
A group around Stephen Plymate incubated human liver cells with insulin for 72 hours. SHBG production fell by around 28 percent, and insulin additionally blocked the SHBG raising effect of estradiol. For you this means: the direction is clear in the lab, but it comes from a petri dish and not from your everyday life.
Plymate SR et al., J Clin Endocrinol Metab 1988. DOI: 10.1210/jcem-67-3-460 · PMID: 2842359 [In vitro]Twenty years later it got more precise. And more interesting.
David Selva and colleagues gave glucose and fructose to transgenic mice carrying the human SHBG gene, and to liver cells. Both sugars lowered SHBG production in a dose dependent way, and they did so through fat synthesis in the liver: the palmitate that forms pushes down HNF-4alpha, the master switch of the SHBG gene. For you this means: SHBG is less a hormone value than a liver value, and fructose gets a role of its own here.
Selva DM et al., J Clin Invest 2007. DOI: 10.1172/JCI32249 · PMID: 17992261 [In vitro] and [In vivo, mouse]Glucose and fructose
arrive in the liver
Lipogenesis rises
palmitate is newly formed
HNF-4alpha falls
the SHBG switch turns down
SHBG falls
less transport protein in the blood
Free hormone rises
testosterone and estradiol act more strongly
Chain one: the switch sits in the liver, not in the gonad.
Does this count in humans? Two large papers argue that it does.
Eric Ding and colleagues compared 359 women with newly diagnosed type 2 diabetes against 359 controls and repeated the analysis in 170 men. In the highest SHBG quartile, diabetes risk was clearly lower, with odds ratios between 0.04 and 0.16 in the women. For you this means: a low SHBG is one of the strongest known early markers of glucose metabolism.
Ding EL et al., N Engl J Med 2009. DOI: 10.1056/NEJMoa0804381 · PMID: 19657112 [Cohort, n=1,058]John Perry and colleagues used a gene variant near the SHBG gene as a natural experiment across 86,138 people. The SHBG raising allele went along with a lower risk of type 2 diabetes, and the observed effect matched the expected one almost exactly. For you this means: a correlation turns into a solid working hypothesis about cause.
Perry JRB et al., Hum Mol Genet 2009. DOI: 10.1093/hmg/ddp522 · PMID: 19933169 [Meta-analysis, k=15, n=86,138]The mechanism comes from cell culture and a mouse model, the human evidence is epidemiological. So far no nutrition study shows that a lowered glycemic load raises SHBG. The chain is well argued, the final step of proof is missing.
Now you can see why a low SHBG often says more about the liver than about the gonad.
Chain one in women: when insulin has a say in the ovaries
Irregular cycle. Hairs on the chin. Acne that never fully went away after puberty. And at some point the sentence: probably PCOS. What often follows is confusion, because suddenly everyone talks about insulin although you came because of your hormones.
There is a peculiarity behind this. In PCOS the ovaries often stay sensitive to insulin, even when muscle and liver no longer are. Picture an apartment where most people no longer hear the doorbell, but one room still does. Ringing louder floods exactly that room.
John Nestler and Daniela Jakubowicz lowered insulin release with medication in women with PCOS over four to eight weeks, against placebo. The insulin area under the curve nearly halved, LH and free testosterone fell clearly, and SHBG rose from 0.8 to 2.3 micrograms per deciliter. For you this means: when the insulin signal comes down, both ends of the chain can move together.
Nestler JE, Jakubowicz DJ, N Engl J Med 1996. DOI: 10.1056/NEJM199608293350902 · PMID: 8687515 [RCT, n=24]One point matters here: that was a medication, not a change in diet. The study shows physiology, not your meal plan. For nutrition there is a separate paper.
Kate Marsh and colleagues compared a low glycemic diet against a conventional healthy diet with identical macronutrients in overweight women with PCOS. At the same weight loss, insulin sensitivity improved more, and 95 percent reported a more regular cycle against 63 percent. For you this means: how fast your blood sugar rises can move the cycle too.
Marsh KA et al., Am J Clin Nutr 2010. DOI: 10.3945/ajcn.2010.29261 · PMID: 20484445 [RCT, n=96]An honest addition belongs here: in both study arms, 49 percent dropped out. That says something about how hard such changes are in everyday life.
Your ovaries have not gone out of rhythm. They hear a signal that has grown too loud, and they answer it very correctly.
That shifts the focus: away from the question of what is wrong with the organ, towards the question of how loud the insulin signal currently is.
Diagnosis and treatment paths I describe in PCO syndrome and in insulin resistance and hormones in women. Here it stays with the mechanism.
That makes it understandable why blood sugar comes up so often in PCOS.
Chain one in men: fat tissue as a hormone organ of its own
The belly has grown over the years, the energy has gone down, the libido too. At the family doctor it sounds like this: testosterone in the lower third of the range, still acceptable. Many men know this conversation.
Fat tissue is not a storage room, it is an active hormone organ. It contains aromatase, an enzyme that converts androgens into estrogen. Picture a conversion plant in the middle of the depot. The larger the depot, the more conversion capacity can stand ready.
Fozia Ahmed and colleagues examined aromatase in subcutaneous fat of men with obesity or type 2 diabetes. It was more strongly expressed and correlated with measures of obesity, high glucose values and insulin resistance, and in the tissue experiment estradiol lowered insulin dependent glucose uptake. For you this means: the conversion plant runs harder with more fat mass, and its product acts locally.
Ahmed F et al., J Clin Endocrinol Metab 2025. DOI: 10.1210/clinem/dgaf038 · PMID: 39833659 [Cohort] and [In vitro]Online you often read: more belly fat equals more aromatase equals more estrogen in the blood. Exactly that last link is what the 2025 paper did not find.
More likely is a local event: the estrogen forms in the tissue and works there, without showing up in the blood panel. Less convenient than the simple version, but closer to the data.
What does move measurably with weight loss is well documented.
Giovanni Corona and colleagues evaluated 24 papers that had measured weight loss and sex hormones in men. On a calorie reduced diet, total testosterone rose by 2.87 nmol/L, after bariatric surgery by 8.73 nmol/L, and in both cases estradiol fell. For you this means: fat mass itself can shape the hormone situation.
Corona G et al., Eur J Endocrinol 2013. DOI: 10.1530/EJE-12-0955 · PMID: 23482592 [Meta-analysis, k=24]The full breadth you will find in estrogen in men and in excess weight, insulin resistance and testosterone. Here only the connection to blood sugar counts: same chain, different place.
So it becomes understandable why waist circumference and hormone panel belong together in men, without a simple equation.
Chain two: the dip counts more than the peak
Back to half past three. Shaky, irritable, a yawn that will not stop, and that very specific craving for something sweet.
What happens there follows a set sequence. When blood sugar falls, your body responds in stages, and each stage has its own threshold. They have been measured for decades.
The four thresholds of counter regulation
81 mg/dL
65 to 68 mg/dL
54 mg/dL
47 mg/dL
Philip Cryer summarized at which value a healthy body answers falling blood sugar. The thresholds are reproducible, but movable: after repeated lows they shift downward. For you one number is the decisive one: cortisol can rise before you notice anything at all.
Cryer PE, Horm Metab Res 1997. DOI: 10.1055/s-2007-978997 · PMID: 9137976 [Mechanism Review]And then came the paper that shifted my view.
Patrick Wyatt, Sarah Berry and colleagues had 1,070 healthy people wear sensors and log more than 80,000 meals. It was not the height of the peak that predicted later behavior, but the depth of the dip 2 to 3 hours afterwards: more hunger and more energy taken in over 24 hours. For you this means: the interesting number sits in the valley, not on the summit.
Wyatt P et al., Nat Metab 2021. DOI: 10.1038/s42255-021-00383-x · PMID: 33846643 [Cohort, n=1,070]Fast peak
a lot of glucose in a short time
Strong insulin answer
the body overshoots slightly
Deep dip
2 to 3 hours after eating
Counter regulation
adrenaline, glucagon, cortisol
Hunger and next peak
the loop starts over
Chain two: repeated cycles mean repeated counter regulation, and cortisol can run along with it.
The cortisol thresholds come from hypoglycemia research, and an ordinary afternoon dip mostly stays above them. Whether it triggers the same cortisol answer has not been measured directly.
The sensor study in turn measured behavior, not cortisol, with correlations between 0.14 and 0.27. What I describe here is a plausible pattern, not a proven causal chain.
The practical levers against steep peaks are in avoiding blood sugar spikes, the path to your own curve in 14 days with a glucose sensor.
That explains why the afternoon is often harder work than lunch was.
How the loop closes: cortisol, belly fat and insulin
A sentence I hear often: I am not eating more than before, and still the belly grows. Usually a second one follows: and my sleep has got worse too.
The two belong together. Cortisol is not only a stress hormone, it is a distribution hormone. It has a say in where energy goes and where it is parked.
Jonathan Purnell and colleagues measured the cortisol production rate over 24 hours and compared it with fat in the abdominal cavity, subcutaneous fat and insulin sensitivity. A higher cortisol production went along with more intra abdominal fat and lower insulin sensitivity, but not with subcutaneous fat. For you this means: the deep fat depot appears to have a relationship of its own with the stress axis.
Purnell JQ et al., Am J Physiol Endocrinol Metab 2009. DOI: 10.1152/ajpendo.90769.2008 · PMID: 19050176 [Cohort, n=24]Elissa Epel and colleagues put women with high and low waist to hip ratios under controlled stress on four days in a row. The women with a central fat pattern released more cortisol, and the lean ones among them had still not got used to it by day three. For you this means: this pattern does not hang on weight alone.
Epel ES et al., Psychosom Med 2000. DOI: 10.1097/00006842-200009000-00005 · PMID: 11020091 [Cohort, n=59]Per Björntorp drew the frame for this in 1991: free fatty acids from visceral fat cells favour insulin resistance in muscle and liver, and the receptor density of the fat depots might explain why energy preferentially travels into the abdominal cavity [Mechanism Review].
Blood sugar swings can call in cortisol. Cortisol can favour visceral fat. Visceral fat can lower insulin sensitivity. And poorer insulin sensitivity can make the next blood sugar swings larger. No beginning, no end, but many places to step in.
Both papers are cross sectional observations, they show associations and not causes. And one detail is uncomfortable: after weight loss, cortisol production even rose relative to the remaining fat mass.
The stress physiology itself I go into in cortisol and the HPA axis in burnout and in cortisol, stress and female hormones. How inflammation joins in is in fries or banana.
And so you can see why this loop feels so stubborn, even though nothing dramatic happens at any single point.
Chain three: what happens to estrogen after it has docked
About estrogen usually only one question gets asked: how much is there? Hardly anyone asks the second one. Where does it go once it has done its work?
In the liver, estrogen is rebuilt in two steps and made water soluble, then it goes through the bile into the gut. Picture a sealed parcel. In the gut sit bacteria that can break the seal open again.
Samantha Ervin and Matthew Redinbo tested 35 bacterial beta-glucuronidases from the gut for whether they can release conjugated estrone and estradiol again. Certain enzyme classes could do it, the reactivation could be inhibited, and the matching inhibitor still did not reduce tumour development in the mouse model. For you this means: the estrobolome exists in a biochemically demonstrable way, a clinical benefit from it has not been shown so far.
Ervin SM et al., J Biol Chem 2019. DOI: 10.1074/jbc.RA119.010950 · PMID: 31636122 [In vitro] and [In vivo, mouse]The popular narrative goes: dysbiosis means more beta-glucuronidase, so more estrogen brought back. The specialist literature partly argues the exact opposite. A widely cited review describes that with lower microbial diversity, less is deconjugated [Mechanism Review].
Both directions are conceivable depending on the starting point. Anyone selling one of them as settled is oversimplifying.
A 2024 review adds: glucuronidase activity in stool depends on nutrition, and on a fat and protein rich diet it is higher than on a fiber rich one. And whether phytoestrogens from soy turn into equol in you is decided by your gut flora [Mechanism Review].
Fiber: plausible, but inconsistent
Barry Goldin and colleagues studied 20 premenopausal women four times over more than a year. The vegetarian women ate 28 instead of 12 grams of fiber, excreted more estrogen in stool, had lower plasma levels and lower beta-glucuronidase activity. For you this means: here fiber, gut enzyme and blood value hang together in one study for the first time.
Goldin BR et al., N Engl J Med 1982. DOI: 10.1056/NEJM198212163072502 · PMID: 7144835 [Cohort, n=20]David Rose and colleagues raised fiber intake from around 15 to 30 grams a day, once with wheat bran, once with oat bran, once with corn bran. After two months, estrone and estradiol fell only in the wheat bran group. For you this means: fiber is not one single substance, the type of fiber appears to have a say.
Rose DP et al., Am J Clin Nutr 1991. DOI: 10.1093/ajcn/54.3.520 · PMID: 1652197 [Cohort, n=62]The methodologically cleanest paper on this is a randomized trial with 213 women over twelve months: low fat, high fiber, plenty of fruit and vegetables. Estradiol fell by 7.5 percent, in the control group by 0.9 percent. The difference was not significant, and SHBG did not move at all.
That is why I phrase chain three as mechanistically plausible and inconsistent in human evidence. Not as documented.
That leaves the cruciferous vegetables. The best study on them is also a warning.
Cynthia Thomson and colleagues gave DIM, a breakdown product from cruciferous vegetables, or placebo in a double blind design. The ratio of estrogen metabolites in urine shifted clearly and SHBG rose by 25 nmol/L, breast density did not change, and blood levels of the tamoxifen metabolites fell significantly. For you this means: substances from cruciferous vegetables can shift estrogen metabolism, and high dose extracts can interact with medication.
Thomson CA et al., Breast Cancer Res Treat 2017. DOI: 10.1007/s10549-017-4292-7 · PMID: 28560655 [RCT, n=130]How the two liver phases work in detail is in lowering estrogen naturally.
Now it makes sense why gut and liver belong in an article about hormones.
Chain four: when too little is hormonally more expensive than too much
You did everything right. Ate cleanly, moved a lot, cut sugar. And then your period stayed away. This is where I get most direct.
Because your brain has its own pacemaker for reproduction: GnRH pulses from the hypothalamus that set the LH rhythm. This rhythm follows available energy more than it follows your weight.
Anne Loucks and Jean Thuma set energy availability precisely over five days in menstruating women and then drew blood every ten minutes for 24 hours. At 30 kilocalories per kilogram of fat free mass per day, LH pulsatility stayed unchanged, below that the pulse frequency fell. For you this means: the response is not a slide, it has a threshold, and cortisol moved along with it.
Loucks AB, Thuma JR, J Clin Endocrinol Metab 2003. DOI: 10.1210/jc.2002-020369 · PMID: 12519869 [RCT, n=29]A second finding comes on top, and it concerns the thyroid.
Stephen Spaulding and colleagues put participants on randomized 800 kilocalorie diets with differing carbohydrate content. Without carbohydrates, T3 fell by 47 percent over two weeks, with at least 50 grams it stayed unchanged at the same calorie count. For you this means: what the calories are made of might have a say in thyroid conversion.
Spaulding SW et al., J Clin Endocrinol Metab 1976. DOI: 10.1210/jcem-42-1-197 · PMID: 1249190 [RCT]This study is from 1976, small, and it ran in people with obesity under strong calorie restriction. The direction is consistent, how far it transfers is open. Since 2023 the consensus statement of the International Olympic Committee stresses the role of low carbohydrate availability, names men as equally affected, and separates problematic from adaptive under fuelling [Systematic Review].
An absent or strongly changed period belongs in medical assessment. Functional hypothalamic amenorrhea is, according to the Endocrine Society guideline, a diagnosis of exclusion [Systematic Review]. Possible consequences include bone density loss and fertility problems.
This is not a topic for a solo nutrition experiment. If you find yourself at this point: below this article you will find the option to book an appointment.
How fasting and the cycle interact is in fasting in women, the cycle phases in cycle based nutrition, the thyroid side in thyroid and female hormones.
That makes it clear why eating less is not automatically the calmer option.
Where these four chains hold and where they get thin
I write this section deliberately, because it is missing from many texts on the topic. Mechanistically, much is well described. What happens when people change their nutrition and hormones are then measured is more inconsistent.
| Chain | What is well documented | Where it gets thin |
|---|---|---|
| 1. Insulin and SHBG | Mechanism worked out in cells and mice, strong epidemiological and genetic human data | No nutrition study has so far shown that a lowered glycemic load raises SHBG |
| 1b. PCOS and aromatase | Lowering insulin moves androgens and SHBG, weight loss moves testosterone and estradiol | More aromatase in fat tissue did not go along with more estradiol in the blood |
| 2. Dip and cortisol | Thresholds precisely measured, dips predict eating behavior | Whether ordinary afternoon dips raise cortisol measurably has not been studied directly |
| 3. Estrobolome and fiber | The enzymes demonstrably exist, a fiber rich diet goes along with lower glucuronidase activity | Largest randomized trial: 7.5 percent decrease without significance, direction disputed |
| 4. Energy availability | Threshold for LH pulsatility shown in a randomized design, guideline available | T3 data from a small 1976 paper in people with obesity |
What follows from this? Above all an attitude: measure instead of guess. The blood sugar curve is the part of these chains that you can most readily make visible in yourself. Not as self optimization, but as a map. What that looks like is in what a CGM sensor shows.
Between the bite and the messenger molecule sit liver, fat tissue, adrenal gland and gut. Looking only at the gonad means looking at the last stop of a long route.
I deliberately name no target values for lab parameters. Reference ranges read differently depending on the lab, your age and your cycle phase, and a number without context creates more unease than clarity. What makes sense in your case belongs in a conversation with your doctor.
And with that you have a map on which you can see which question is worth asking for you.
Common questions about nutrition, blood sugar and hormones
Can nutrition really influence my hormones, or is that marketing?
Both happen, and it depends on the size of the promise. It is well documented that glucose metabolism and sex hormones are tightly coupled: in the Women's Health Study, diabetes risk in the highest SHBG range was more than 90 percent lower than in the lowest. It is also documented that a low glycemic diet in PCOS improved cycle regularity more than a conventional healthy diet, at identical weight loss. What is not documented is that single hormone values can be steered by a particular food. Nutrition shifts probabilities, it does not set values.
What is SHBG, and why is a low value a warning sign?
SHBG stands for sex hormone binding globulin. It is built in the liver and binds testosterone and estradiol in the blood. When SHBG falls, the freely available share of both hormones rises, without the total values having to change much. What makes SHBG interesting above all is its role as a metabolic marker: in a case control analysis, diabetes risk in the highest quartile was clearly lower, and a genetic analysis across 15 studies and 86,138 people supports a causal share. What your personal value means belongs in a conversation with your doctor.
At what blood sugar level does the body release cortisol?
According to the classic threshold work by Philip Cryer, the response runs in a set sequence. Insulin release falls at around 4.5 mmol/L, that is 81 mg/dL. Counter regulation with glucagon, adrenaline, growth hormone and cortisol begins at around 3.6 to 3.8 mmol/L, that is 65 to 68 mg/dL. Noticeable symptoms only arrive at around 3.0 mmol/L. So cortisol can respond before you feel anything. One point of context matters: these numbers come from hypoglycemia research and not from studies of ordinary afternoon dips.
Is the blood sugar peak or the dip afterwards more important?
In the largest study on this, 1,070 people wore a glucose sensor. The dip 2 to 3 hours after eating predicted later eating behavior better than the peak: more hunger, a shorter gap to the next meal and more energy taken in over 24 hours. The associations were weak to moderate, with correlations between 0.14 and 0.27. They describe a pattern, not an inevitability. In practice this means the question is not only how high you go, but how you come back down.
Why do I crave sweets before my period?
In a sensor study with 49 people across 149 cycles, mean daily glucose was highest in the luteal phase and lowest in the late follicular phase. Higher daily estrogen levels went along with lower glucose values, more reported craving with higher ones. That fits what many women already observe in themselves. It is an observational study though, so it does not establish a cause. And it turns a common narrative around, because estrogen here pointed towards the calmer glucose situation.
Do blood sugar swings make belly fat, or is it the other way round?
Probably both, and that is exactly what makes the loop so stubborn. In 24 men, a higher cortisol production rate correlated with more intra abdominal fat and with lower insulin sensitivity, but not with subcutaneous fat. In 59 women, even the lean ones with a central fat pattern showed the stronger cortisol response, and they did not get used to the stress over three days. Both papers are cross sectional observations. They show a connection, not a clear direction.
Do sugar and belly fat give men more estrogen?
It is not that simple. Fat tissue contains aromatase, the enzyme that converts androgens into estrogen, and in men with obesity it is more strongly expressed. In the most recent tissue study, however, no association was found between the amount of aromatase in fat tissue and estradiol in the blood. The link seems to sit locally in the tissue rather than systemically. What is well documented is the other direction: in a meta-analysis of 24 studies, total testosterone rose by 2.87 nmol/L after diet and by 8.73 nmol/L after bariatric surgery, while estradiol fell.
What is the estrobolome, and can I influence it through nutrition?
The estrobolome refers to the genes of gut bacteria that can reactivate estrogen. In 2019, work on 35 isolated gut enzymes showed for the first time which of them actually release conjugated estrone and estradiol again. A recent review also describes that glucuronidase activity in stool is lower on a fiber rich diet than on a fat and protein rich one. The direction of the effect is disputed in the literature, because with low microbial diversity less estrogen may return to circulation as well. I would not derive a control manual from this.
Does fiber lower estrogen levels?
Partly, and the data are inconsistent. Vegetarian women eating 28 instead of 12 grams of fiber per day excreted more estrogen in stool and had lower plasma levels. In an intervention study with 62 women, however, only wheat bran lowered estrone and estradiol, oat and corn bran did not. And the largest randomized trial with 213 women found only a 7.5 percent decrease over twelve months, without statistical significance. Mechanistically plausible, so far weak in human evidence.
What about broccoli, cabbage and DIM capsules?
In a randomized trial with 130 women on tamoxifen, DIM, a breakdown product from cruciferous vegetables, clearly shifted the ratio of estrogen metabolites in urine, and SHBG rose by 25 nmol/L against practically no change on placebo. Breast density did not change on mammography or MRI. One finding belongs with this: blood levels of the tamoxifen metabolites fell significantly. That is a clear interaction signal. Anyone taking medication should therefore have high dose cruciferous extracts checked medically. Vegetables on your plate are explicitly not what is meant here.
Can low carb or intermittent fasting stop my cycle?
That can happen. In a randomized crossover trial with 29 women, LH pulsatility stayed unchanged at an energy availability of 30 kilocalories per kilogram of fat free mass per day. Below that, pulse frequency fell and amplitude rose. In an older randomized study, T3 fell by 47 percent on a carbohydrate free 800 kilocalorie diet, but stayed unchanged at the same calorie count with at least 50 grams of carbohydrate. An absent or strongly changed period belongs in medical assessment. Functional hypothalamic amenorrhea is, according to the guideline, a diagnosis of exclusion.
Which blood values are worth looking at if I want to examine this connection in myself?
What helps most is looking at glucose metabolism and hormones in the same picture instead of separately. In the literature, fasting insulin, SHBG, free and total testosterone, estradiol and a daily cortisol profile keep coming up. I deliberately name no target values here, because reference ranges read differently depending on the lab, your age, your cycle phase and the question being asked. Which values contribute anything at all in your case, and how to read them, belongs in a conversation with your doctor and not in a general list.
Nutrition and hormones in a wider context
The four chains do not end at the nutrition topic. They run on into weight regulation, stress physiology and the thyroid.
Leptin and insulin
The hormones that help steer your weight
What a CGM shows
Measuring instead of guessing, on your own curve
Cortisol and the HPA axis
When the stress axis stays dysregulated
Thyroid and hormones
The link to chain four and T3 conversion
Scientific sources
- Plymate SR, Matej LA, Jones RE, Friedl KE. Inhibition of sex hormone-binding globulin production in the human hepatoma (Hep G2) cell line by insulin and prolactin. J Clin Endocrinol Metab. 1988;67(3):460-4. DOI: 10.1210/jcem-67-3-460 · PMID: 2842359 [In vitro]
- Selva DM, Hogeveen KN, Innis SM, Hammond GL. Monosaccharide-induced lipogenesis regulates the human hepatic sex hormone-binding globulin gene. J Clin Invest. 2007;117(12):3979-87. DOI: 10.1172/JCI32249 · PMID: 17992261 [In vitro] and [In vivo, mouse]
- Ding EL, Song Y, Manson JE et al. Sex hormone-binding globulin and risk of type 2 diabetes in women and men. N Engl J Med. 2009;361(12):1152-63. DOI: 10.1056/NEJMoa0804381 · PMID: 19657112 [Cohort, n=1,058]
- Perry JRB, Weedon MN, Langenberg C et al. Genetic evidence that raised sex hormone binding globulin levels reduce the risk of type 2 diabetes. Hum Mol Genet. 2009;19(3):535-44. DOI: 10.1093/hmg/ddp522 · PMID: 19933169 [Meta-analysis, k=15, n=86,138]
- Nestler JE, Jakubowicz DJ. Decreases in ovarian cytochrome P450c17 alpha activity and serum free testosterone after reduction of insulin secretion in polycystic ovary syndrome. N Engl J Med. 1996;335(9):617-23. DOI: 10.1056/NEJM199608293350902 · PMID: 8687515 [RCT, n=24]
- Marsh KA, Steinbeck KS, Atkinson FS, Petocz P, Brand-Miller JC. Effect of a low glycemic index compared with a conventional healthy diet on polycystic ovary syndrome. Am J Clin Nutr. 2010;92(1):83-92. DOI: 10.3945/ajcn.2010.29261 · PMID: 20484445 [RCT, n=96]
- Ahmed F, Hetty S, Laterveer R et al. Altered Expression of Aromatase and Estrogen Receptors in Adipose Tissue From Men With Obesity or Type 2 Diabetes. J Clin Endocrinol Metab. 2025;110(10):e3410-e3424. DOI: 10.1210/clinem/dgaf038 · PMID: 39833659 [Cohort] and [In vitro]
- Corona G, Rastrelli G, Monami M et al. Body weight loss reverts obesity-associated hypogonadotropic hypogonadism: a systematic review and meta-analysis. Eur J Endocrinol. 2013;168(6):829-43. DOI: 10.1530/EJE-12-0955 · PMID: 23482592 [Meta-analysis, k=24]
- Cryer PE. Hierarchy of physiological responses to hypoglycemia: relevance to clinical hypoglycemia in type I diabetes mellitus. Horm Metab Res. 1997;29(3):92-6. DOI: 10.1055/s-2007-978997 · PMID: 9137976 [Mechanism Review]
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