Appetite Hormones and Hyperemesis Gravidarum

The Hidden Battle Within Pregnancy

When Normal Pregnancy Symptoms Turn Severe

Pregnancy is often portrayed as a time of joyful anticipation, but for up to 3.6% of expectant mothers, this experience is dramatically different 6 . These women face hyperemesis gravidarum (HG) - a severe form of nausea and vomiting that extends far beyond typical "morning sickness."

3.6%

of pregnant women affected by HG 6

5-10%

weight loss common in severe cases 7

#1 Cause

of first-trimester hospitalization 7

Unlike ordinary pregnancy nausea that comes and goes, HG involves prolonged, severe symptoms that can lead to dehydration, significant weight loss, and nutritional deficiencies 6 7 . Recent research has begun to uncover a fascinating explanation for this debilitating condition: the same appetite-regulating hormones that normally help control our food intake appear to be playing a disruptive role in HG.

The Science of Appetite: Your Body's Natural Regulators

To understand what goes wrong in hyperemesis gravidarum, we must first appreciate how appetite regulation normally works. Our bodies maintain a sophisticated communication system between our gut and brain, orchestrated by specialized hormones that signal when to eat and when to stop 1 .

The Key Players in Your Gut-Brain Dialogue

Ghrelin

The only known "hunger hormone" produced primarily in the stomach. Its levels rise before meals, triggering feelings of hunger, and fall sharply after eating 1 .

Increases Appetite
GLP-1

An appetite-suppressing hormone secreted from intestinal L-cells after eating. It promotes feelings of fullness and helps regulate blood sugar 1 .

Decreases Appetite
PYY

Another satiety signal released from intestinal L-cells that provides sustained feelings of fullness after meals 1 .

Decreases Appetite
CCK

One of the earliest discovered satiety hormones, responsible for the initial feeling of fullness during a meal 1 .

Decreases Appetite

Hormone Functions at a Glance

Hormone Origin Primary Function Effect on Appetite
Ghrelin Stomach Hunger initiation Increases (Orexigenic)
GLP-1 Intestinal L-cells Meal termination, blood sugar regulation Decreases (Anorexigenic)
PYY Intestinal L-cells Sustained satiety Decreases (Anorexigenic)
CCK Upper intestine Early satiation Decreases (Anorexigenic)

The Perfect Storm: Appetite Hormones in Hyperemesis Gravidarum

Pregnancy creates a hormonal environment unlike any other life stage, and for women susceptible to HG, this transformation becomes particularly extreme. Researchers have identified several key biological factors that contribute to this condition.

The GDF15 Connection

One of the most significant discoveries in understanding HG comes from research on Growth Differentiation Factor 15 (GDF15), a hormone that appears to play a central role in triggering severe nausea and vomiting during pregnancy 7 .

Under normal circumstances, GDF15 is involved in signaling stress responses, but during pregnancy, its levels can become dramatically elevated. Interestingly, sensitivity to GDF15 seems to be a crucial factor - it's not just the amount of the hormone present, but how a woman's body responds to it that may determine whether she develops HG 6 .

The Gut Hormone Imbalance

Beyond GDF15, researchers are exploring how traditional appetite hormones become dysregulated in HG:

  • Ghrelin disruption: The normal hunger-signaling function of ghrelin may be disrupted, preventing appropriate hunger cues at times when nourishment is critically needed 1 .
  • Enhanced satiety signaling: There may be an exaggerated response to satiety hormones like GLP-1 and PYY, causing the body to trigger "fullness" and nausea signals prematurely or excessively 1 .
  • hCG interactions: The pregnancy hormone human chorionic gonadotropin (hCG), which rises dramatically in early pregnancy, may stimulate thyroid hormone production and interact with appetite regulatory pathways in ways that promote nausea and vomiting 7 .

This complex hormonal interplay creates a devastating cycle: the body's natural systems for regulating food intake become overactive, making the thought, smell, or consumption of food trigger nausea rather than pleasure or nourishment.

Hormonal Changes in Normal Pregnancy vs. HG

*Illustrative representation based on research findings

Beyond Physical Suffering: The Neuropsychiatric Toll of HG

The impact of hyperemesis gravidarum extends far beyond physical symptoms. Groundbreaking research has revealed that women with HG face significantly increased risks of numerous neuropsychiatric and mental health conditions 6 .

Key Findings from a Study of 476,857 Pregnant Women
More than 50% increased risk

for 13 different neuropsychiatric conditions

Doubled risk

for Wernicke's encephalopathy, refeeding syndrome, eating disorders, and depression

Postpartum depression

occurring 2.7 times more frequently in women with HG

Increased risk

of postpartum psychosis and post-traumatic stress disorder 6

Perhaps most surprisingly, researchers found that the internationally recognized categorization of HG based on metabolic disturbance (viewed as more medically severe) showed reduced risk of depression compared to mild HG. This counterintuitive finding highlights that the severity of metabolic symptoms doesn't directly correlate with mental health impact 6 .

The severity of HG does not directly correlate with the degree of impact on mental health, and as clinicians, we have a responsibility to ensure these women receive adequate integrated care across both physical and mental health.

Dr. Hamilton Morrin, researcher at King's College London 6

A Glimpse into the Research: The MOTHER Trial

To better understand how research into HG is conducted, let's examine a crucial study that investigated this condition and its potential interventions.

MOTHER Trial Overview
Study Design

The MOTHER randomized controlled trial (Maternal and Offspring outcomes after Treatment of HyperEmesis by Refeeding) was designed to evaluate whether early enteral tube feeding could benefit women hospitalized with HG 3 .

Participants

The study included 215 women: 115 participated in the randomized trial, while 100 were part of an observational cohort.

Data Collection
Symptom severity using PUQE-24 score
Nutritional intake via 24-hour food diaries
Maternal weight changes
Cord blood samples at delivery

Key Findings from the MOTHER Trial

Primary Finding

Enteral tube feeding in addition to standard care did not significantly affect symptoms or birth outcomes 3 .

Metabolic Associations

Lower maternal weight gain was associated with higher cord blood glucose and Apo-B levels in offspring, suggesting potential metabolic changes 3 .

HG Severity and Offspring Cord Blood Markers
HG Severity Measure Cord Blood Marker Association Found Clinical Significance
Maternal weight gain Glucose Inverse correlation Lower weight gain linked to higher offspring glucose
Maternal weight gain Apo-B Inverse correlation Lower weight gain linked to higher Apo-B (cardiovascular risk marker)
Severity of vomiting All markers No significant association Symptom severity not directly linked to these cord blood markers
24-hour energy intake All markers No significant association Short-term nutritional intake not predictive of these outcomes
Hospital admission duration All markers No significant association Healthcare utilization not correlated with these markers

Future Directions: Hope on the Horizon

Research into appetite hormones and HG continues to evolve, with several promising avenues emerging:

Genetic Discoveries

Recent genetic studies have identified two promising drug targets for HG: OVGP1 and LGALS1 4 .

Using a method called Mendelian randomization, researchers found that these two blood drug targets showed significant results in two independent datasets 4 .

Even more encouraging, further analysis revealed that targeting these genes doesn't appear to increase risks for adverse pregnancy outcomes or other common diseases, making them particularly attractive for future drug development 4 .

The GIP and GLP-1 Connection

Research into gastric inhibitory peptide (GIP), another gut hormone, reveals fascinating possibilities.

While GLP-1 receptor agonists frequently cause nausea as a side effect, combining them with GIP may offer a better approach 2 .

Surprisingly, GIP receptor activation appears to have antiemetic properties - meaning it may reduce nausea and vomiting 2 .

This discovery has led to the development of dual GIP/GLP-1 receptor agonists that might provide the benefits of these hormones while minimizing the nausea that typically limits their use 2 .

Research Tools in Appetite Hormone Studies

Research Tool Primary Function Application in HG Research
Genetic instrumental variables Identify causal relationships Used in Mendelian randomization to discover drug targets 4
PUQE-24 score Quantify symptom severity Standardized measurement of nausea/vomiting severity in clinical studies 3
Cord blood analysis Assess offspring metabolic markers Evaluate long-term impacts of HG on offspring health 3
Hormone infusion studies Determine hormone effects Establish causal relationships between specific hormones and symptoms 1
Dual GIP/GLP-1 receptor agonists Combined hormone therapy Investigate potential treatments that maximize benefits while minimizing nausea 2

Toward Better Understanding and Treatment

The exploration of appetite hormones in hyperemesis gravidarum represents a fascinating convergence of endocrinology, genetics, and clinical medicine.

Once dismissed as merely psychological, HG is now recognized as a complex biological disorder rooted in the very systems that normally ensure our adequate nourishment. As research continues to unravel the intricate hormonal dance that goes awry in this condition, new hope emerges for more effective, targeted treatments that might one day relieve the suffering of hundreds of thousands of women worldwide.

Until recently, there has been something of a disconnect between how the medical community has regarded the mental health impact of HG and how women themselves describe their experience. Our findings show that this gap is not only real but can be very serious.

Dr. Thomas Pollak, neuropsychiatrist involved in HG research 6

References