Introduction

Traumatic brain injury (TBI) and concussion, has far-reaching physiological effects beyond immediate cognitive and neurological impairment. One of the most underrecognized yet clinically significant consequences of brain injury is its impact on the endocrine system. The brain, especially the hypothalamus and pituitary gland, plays a central role in regulating hormonal balance. Damage to these areas—commonly referred to as the hypothalamic-pituitary axis (HPA)—can disrupt hormone production, secretion, and regulation, often leading to persistent symptoms that are mistakenly attributed to psychological or structural causes alone.

This article explores the hormonal disturbances that can result from brain injury, the prevalence and mechanisms behind post-traumatic hypopituitarism (PTHP), and provides guidance on which hormones should be assessed in clinical practice.

The Hypothalamic-Pituitary Axis and Brain Injury

The hypothalamus and pituitary gland act as master regulators of the endocrine system. They coordinate the release of multiple hormones critical to metabolism, growth, stress response, mood, sexual function, and fluid balance. TBI can impair these regulatory functions through direct trauma, inflammation, edema, vascular damage, or delayed regeneration of the HPA structures.

Types of Brain Injury That Affect Hormonal Balance

• Mild TBI (Concussion)
• Moderate to Severe TBI
• Repetitive Head Trauma (e.g., athletes, military personnel)

Even mild injuries can lead to significant hormonal disruption, especially if repeated over time (e.g., in contact sports) [1].

Prevalence of Post-Traumatic Hormonal Imbalances

Numerous studies show that hormonal imbalances occur in 15–68% of individuals after TBI, depending on injury severity, timing of testing, and diagnostic criteria [2][3].

• Acute phase (first 2 weeks post-injury): transient hormonal changes are common.
• Chronic phase (3 months to several years): permanent dysfunction may persist in up to 25–50% of individuals [4].

A systematic review by Schneider et al. (2007) found that approximately 30% of TBI survivors develop some form of hypopituitarism, with growth hormone deficiency being the most prevalent [2].

Key Hormonal Systems Affected

1. Growth Hormone (GH)

• Prevalence: 15–20% in moderate/severe TBI, 10% in mild TBI [4].
• Symptoms: fatigue, reduced muscle mass, poor exercise tolerance, depression, and cognitive dysfunction.
• Pathophysiology: The somatotropic axis is highly sensitive to injury; the GH-releasing hormone pathway is vulnerable to shear stress.
• Assessment: Serum IGF-1 is a screening tool, but dynamic stimulation tests (e.g., insulin tolerance test or GHRH-arginine test) are more reliable [5].

2. Adrenocorticotropic Hormone (ACTH) and Cortisol

• Prevalence: ACTH deficiency is found in up to 10–20% of individuals [6].
• Symptoms: fatigue, hypotension, nausea, poor stress tolerance, and hyponatremia.
• Timing: Cortisol levels can be acutely suppressed due to stress or permanently due to HPA axis disruption.
• Assessment: Morning serum cortisol; if borderline, perform ACTH stimulation test.

Acute cortisol insufficiency can be life-threatening and requires prompt treatment [7].

3. Thyroid Stimulating Hormone (TSH) and Free T4

• Prevalence: Central hypothyroidism is seen in 5–10% of cases post-TBI [8].
• Symptoms: fatigue, cold intolerance, weight gain, depression, and bradycardia.
• Assessment: TSH and free T4 (note that TSH may be inappropriately normal or low in central hypothyroidism).

Thyroid dysfunction may worsen cognitive outcomes and mood, so screening is essential even for mild TBI.

4. Gonadotropins (LH/FSH) and Sex Hormones (Testosterone, Estradiol)

• Prevalence: Gonadotropin deficiency in up to 20% of men; less frequently studied in women [9].
• Symptoms in Men: low libido, erectile dysfunction, reduced facial/body hair, and muscle loss.
• Symptoms in Women: menstrual irregularities, infertility, low libido, and hot flashes.
• Assessment: LH, FSH, total testosterone (in men), estradiol (in women), and sex hormone-binding globulin (SHBG).

Hormonal imbalance in this axis is associated with depression and reduced quality of life post-injury [10].

5. Prolactin

• Prevalence: Hyperprolactinemia is occasionally observed.
• Mechanism: May occur due to pituitary stalk damage or hypothalamic inhibition of dopamine.
• Symptoms: galactorrhea, infertility, sexual dysfunction.

Testing for prolactin levels is useful in the presence of menstrual or sexual symptoms post-TBI.

6. Antidiuretic Hormone (ADH) and Sodium Balance

• Disorders:
  • Diabetes Insipidus (DI) – deficiency of ADH
  • Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) – excess ADH
• Symptoms: Polyuria, polydipsia, dehydration (DI); hyponatremia, fluid retention (SIADH).
• Assessment: Serum sodium, urine osmolality, plasma osmolality, ADH levels.

These imbalances often occur in the acute phase and can be life-threatening if unrecognized [11].

7. Insulin and glucose metabolism

Following a traumatic brain injury (TBI), including mild forms such as concussions, significant alterations in insulin regulation and glucose metabolism can occur, contributing to both acute and chronic neurological and metabolic consequences. The brain plays a critical role in regulating systemic metabolism, and damage to regions such as the hypothalamus or pituitary gland can disrupt insulin sensitivity and secretion.

Studies have shown that after a TBI, patients may develop insulin resistance, even in the absence of pre-existing metabolic disease. This insulin resistance is thought to arise from neuroinflammation, oxidative stress, and impaired neuronal insulin signaling pathways (15,16).

Prevalence of insulin resistance and dysregulated glucose metabolism: Research indicates that up to 50% of moderate-to-severe TBI patients develop some form of glucose metabolism disturbance, including hyperglycemia or insulin resistance in the acute phase post-injury (17). Moreover, even in cases of mild TBI or concussion, subtle but persistent changes in insulin function have been observed, particularly in individuals with repetitive head injuries, such as athletes.

Long term impact: These changes are associated with increased risk for long-term cognitive decline and neurodegenerative diseases like Alzheimer’s, which are themselves linked to insulin resistance in the brain (18).

Timing of Hormonal Assessment

• Acute phase (first 2–4 weeks): Focus on cortisol and ADH abnormalities.
• Subacute phase (1–3 months): GH, TSH, gonadal hormones should begin to normalize or demonstrate deficiency.
• Chronic phase (>3 months): Full endocrine workup recommended, especially in symptomatic patients.

Repeat testing is important, as some deficiencies are transient while others develop over time [12].

Clinical Symptoms That May Indicate Hormonal Dysfunction

Because symptoms of hormonal deficiency can overlap with post-concussive syndrome (e.g., fatigue, poor concentration, mood swings), clinicians must maintain a high index of suspicion. Red flags include:

• Persistent fatigue and malaise unresponsive to rest
• Sexual dysfunction or amenorrhea
• Weight gain or loss with no lifestyle explanation
• Depression or anxiety that worsens over time
• Cold intolerance, dry skin, or hair thinning
• Hypoglycemia or hypotension

Populations at Higher Risk

• Moderate to severe TBI patients
• Individuals with skull fractures, especially basilar
• Those requiring neurosurgery or ICU admission
• Patients with repetitive mild TBIs (e.g., athletes, veterans)
• Children and adolescents (disruption of growth and puberty)

Athletes with repeated concussions may develop chronic traumatic encephalopathy (CTE), which also involves hormonal changes, particularly low testosterone and GH deficiency [13].

Recommended Hormonal Panel After TBI/Concussion

Hormone	Test	When to Assess
Cortisol	8am serum cortisol ± ACTH stimulation	Acute and chronic
GH axis	IGF-1, GHRH-arginine test	Chronic (>3 months)
Thyroid	TSH, Free T4	Subacute and chronic
Gonadal	LH, FSH, Testosterone/Estradiol	Subacute and chronic
Prolactin	Serum prolactin	If symptoms suggest
ADH	Sodium, osmolality, ADH	Acute phase, if symptomatic
Insulin	Insulin, glucose fasting, HBA1C	Chronic

 

Treatment and Follow-Up

Hormone replacement, nutraceuticals (herbs, supplements, glandulars), diet and lifestyle can significantly improve quality of life and neurocognitive recovery in TBI individuals. Individualized therapy is guided by deficiency severity, patient symptoms, and comorbidities. Referral to an Endocrinologist or Naturopath Doctor is essential for proper diagnosis and dynamic testing.

• GH replacement improves energy, mood, cognition, and body composition [14].
• Cortisol therapy may be life-saving in adrenal insufficiency.
• Thyroid and sex hormone replacement alleviates fatigue, mood issues, and sexual dysfunction.
• Glandulars, herbs and nutrient supplementation can help to balance hormones
• Nutrition and Lifestyle strategies can help to mitigate issues

Conclusion

Brain injury—even mild concussion—can disrupt multiple hormonal pathways, contributing to prolonged or unexplained symptoms. The hypothalamic-pituitary axis is especially vulnerable, and damage may lead to deficiencies in growth hormone, cortisol, thyroid hormones, gonadal hormones, insulin, prolactin, and antidiuretic hormone. Timely endocrine evaluation is critical for optimal management. In patients with persistent symptoms post-concussion, hormonal assessment should be part of the routine workup to prevent misdiagnosis and to enhance recovery outcomes.

If you or you client is interested in completing hormonal testing please reach out to Koru Nutrition for a free discovery call or book in with one of our naturopath doctors.

Or, if you or your client was involved in a motor vehicle accident, then please complete our online referral form so we can complete the OCF-18.

References

 

1. Zgaljardic DJ, et al. (2008). “Neuroendocrine dysfunction after traumatic brain injury: an update on diagnosis and treatment.” Current Opinion in Endocrinology, Diabetes and Obesity, 15(4):301-307. doi:10.1097/MED.0b013e3283064a4f
2. Schneider HJ, et al. (2007). “Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review.” JAMA, 298(12):1429–1438. doi:10.1001/jama.298.12.1429
3. Klose M, et al. (2007). “Prevalence and predictive factors of post-traumatic hypopituitarism.” Clinical Endocrinology, 67(2):193–201. doi:10.1111/j.1365-2265.2007.02873.x
4. Aimaretti G, et al. (2005). “Hormonal deficiencies after traumatic brain injury in humans.” Horm Res, 64(6):293–299. doi:10.1159/000088786
5. Tanriverdi F, et al. (2010). “Pituitary dysfunction after traumatic brain injury: a clinical and pathophysiological approach.” Endocrine Reviews, 31(2): 244–277. doi:10.1210/er.2009-0008
6. Bondanelli M, et al. (2004). “Hypopituitarism after traumatic brain injury.” European Journal of Endocrinology, 152(5):679–691. doi:10.1530/eje.0.1520679
7. Agha A, et al. (2005). “The natural history of post-traumatic hypopituitarism: implications for assessment and treatment.” American Journal of Medicine, 118(12):1416.e1–1416.e7. doi:10.1016/j.amjmed.2005.01.073
8. Schneider M, et al. (2013). “Endocrine dysfunction following TBI: a review.” Journal of Neurotrauma, 30(11):1017–1030. doi:10.1089/neu.2012.2602
9. Urban RJ, et al. (2005). “Hypogonadism after TBI.” Journal of Neurotrauma, 22(11):1141–1147. doi:10.1089/neu.2005.22.1141
10. Wagner AK, et al. (2010). “Biopsychosocial correlates of hypopituitarism after traumatic brain injury.” Brain Injury, 24(3): 297–305. doi:10.3109/02699050903421119
11. Kristof RA, et al. (2009). “Acute changes of the hypothalamic–pituitary–adrenal axis after traumatic brain injury.” European Journal of Endocrinology, 160(1):137–143. doi:10.1530/EJE-08-0612
12. Krahulik D, et al. (2010). “Dynamic changes in hormonal levels in acute phase of TBI.” J Neurosurg Sci, 54(3):77–83.
13. Kelly DF, et al. (2000). “Neuroendocrine dysfunction after traumatic brain injury: a critical review.” Neurosurgery, 47(6):1343–1352. doi:10.1097/00006123-200012000-00003
14. High WM, et al. (2010). “Effect of growth hormone replacement therapy on cognition after traumatic brain injury.” Journal of Neurotrauma, 27(9): 1687–1695. doi:10.1089/neu.2010.1312
15. Bhowmick, S., D’Mello, V., Ponery, N., & Chatterjee, S. (2018). Brain insulin resistance and its link to cognitive dysfunction: Potential implications in traumatic brain injury. Neuropharmacology, 136(Pt B), 190–197. https://doi.org/10.1016/j.neuropharm.2017.11.009
16. Jalloh, I., Helmy, A., Shannon, R. J., Gallagher, C. N., Menon, D. K., & Hutchinson, P. J. (2015). Lactate uptake by the injured human brain: Evidence from an arterio-venous gradient and cerebral microdialysis study. Journal of Neurotrauma, 32(9), 689–699. https://doi.org/10.1089/neu.2014.3675
17. Wagner, A. K., Sokunbi, O. F., Ren, D., Chen, X., Li, Y., & Conley, Y. P. (2017). Controlled cortical impact injury influences insulin signaling pathway gene expression in the brain. Journal of Neurotrauma, 34(5), 1041–1049. https://doi.org/10.1089/neu.2015.4272
18. De Felice, F. G., & Ferreira, S. T. (2014). Inflammation, defective insulin signaling, and mitochondrial dysfunction as common molecular denominators connecting type 2 diabetes to Alzheimer disease. Diabetes, 63(7), 2262–2272. https://doi.org/10.2337/db13-1954

Defining Menopause and Perimenopause

Menopause is officially marked by 12 consecutive months without a menstrual period. This is where estrogen and progesterone production dramatically decreases. Perimenopause is the 7–10 years leading up to menopause, in what can often feels like the “zone of chaos”. This is where woman experience the unpredictable hormone cycles which trigger symptoms such as hot flashes, irregular bleeding, mood swings, frozen shoulders, poor memory, difficulty sleeping and cognitive fog.

Biological and Mental Health Ramifications

As estrogen dips, inflammation increases—leading to higher risks of cardiovascular disease, osteoporosis, arthritis, mood disorders and visceral fat gain. During perimenopause the risk of mood disorders such as anxiety and depression sigificantly increases by around 40% due to hormone-sensitive neurotransmitter disruptions.

Core Symptoms and Health Changes during Perimenopause

• Vasomotor Disturbances: Hot flashes and night sweats are classic: sudden warmth followed by sweating due to dysregulated temperature control.
• Cognitive Dysfunction: “Brain fog”—memory lapses, decision-making difficulties, and focus problems—are common complaints.
• Sleep Disturbances: Hormonal fluctuations lead to insomnia and disturbed sleep, which compound fatigue and mood symptoms as well as cravings and poor food choices.
• Weight and Metabolism: Women in menopause experience body compositional shifts: muscle loss combined with visceral fat gain (rising from ~8% to ~23% body fat in studies) even without lifestyle change. It’s not just weight gain—it’s the location of fat storage that increases metabolic risk.
• Bone & Musculoskeletal Decline: The drop in estrogen accelerates bone thinning and contributes to joint pain, stiffness, and conditions like “frozen shoulder”.
• Metabolic Syndrome & Insulin Resistance: Insulin sensitivity worsens after menopause—raising the risk for metabolic syndrome, type 2 diabetes, and related conditions

Diet and Nutrition: The Anti-Inflammatory Foundation

Woman even those that are fit and health conscious are now finding the things that they were doing before are now no longer working even with increased workouts and reduced caloric intake the weight isn’t budging. Instead, the love handles and muffin top seems to be growing. It can be extremely frustrating and demoralizing. But with those hormonal shifts there also needs to come dietary and exercise shifts to accommodate your new body chemistry.

There are a number of diets that can help with Menopause. These include:

• The Galveston Diet by Dr Mary Claire Haver
• Metabolic Balance Program
• Anti-inflammatory Diet
• Mediterranean Diet

The top two that we will discuss are the Galveston Diet and the Metabolic Balance Program.

The Galveston Diet

Dr. Mary Claire Haver, a board-certified OB-GYN and menopause specialist, developed the Galveston Diet specifically to address the unique metabolic and hormonal challenges women face during perimenopause and menopause. Unlike traditional calorie-restriction diets, the Galveston Diet emphasizes anti-inflammatory nutrition, intermittent fasting, and balanced macronutrient intake, particularly focusing on healthy fats and fiber while reducing refined carbohydrates. Dr. Haver designed the program to counteract common menopausal symptoms such as weight gain, fatigue, and brain fog, which are often linked to hormonal shifts—especially the decline in estrogen. Estrogen plays a vital role in regulating metabolism, insulin sensitivity, and fat distribution, and its loss during menopause often leads to visceral fat accumulation and systemic inflammation (1,2) Lovejoy et al., 2008; Carr, 2003).

One core principle of the Galveston Diet is reducing inflammation through diet. Dr. Haver advocates for a Mediterranean-style eating pattern—rich in omega-3 fatty acids (e.g., from fatty fish, nuts), polyphenols (from berries, olive oil, leafy greens), and whole foods—while eliminating processed and high-sugar items. It focus’ on adequate protein (50–120 g/day depending on lean mass) to maintain muscle and metabolic health and high fiber intake (≥25–32 g/day) to support gut health, improve glycemic control, and reduce visceral fat.

Scientific studies support this anti-inflammatory approach. For example, a Mediterranean diet has been associated with reduced levels of C-reactive protein (CRP) and interleukin-6 (IL-6), two markers of systemic inflammation often elevated during menopause (3). Additionally, menopause-related weight gain has been shown to correlate with increased insulin resistance and chronic inflammation, which can further elevate risks for cardiovascular disease and type 2 diabetes (4). The Galveston Diet’s anti-inflammatory focus may help mitigate these risks.

Another key element of the Galveston Diet is intermittent fasting (IF), particularly the 16:8 method—16 hours of fasting followed by an 8-hour eating window. Research shows that intermittent fasting may improve insulin sensitivity, reduce oxidative stress, and enhance fat metabolism, all of which are particularly beneficial for midlife women experiencing metabolic slowdowns (5). By aligning eating patterns with the body’s circadian rhythms, IF may also improve sleep and energy levels, both commonly disrupted during menopause. There is some controversy on IF with menopausal woman (as it may not work well with everyone). Long-term studies on intermittent fasting in menopausal women are still emerging, initial findings are promising and align with the results Dr. Haver has reported in her clinical observations and patient feedback.

The Metabolic Balance Program

Metabolic Balance®, is a personalized nutrition program developed in Germany in 2001, resets metabolism through individualized meal plans based on 36 blood markers and personal data (e.g., age, medical history, food preferences). This program is base don reducing inflammation and lowering insulin to get into fat burning mode.

Clinical trials—including a long-term study by the Albert Ludwig University of Freiburg’s Medical Center published in the Journal of Nutrition and Metabolism—show that participants lost and maintained significant weight (62.5% lost ≥5%, with 31.1% losing ≥10% of initial weight) for over a year; improvements in blood biomarkers such as cholesterol and insulin and quality-of-life measures were also identified (6). The approach emphasizes real food, no packaged products, and supports metabolic health by regulating insulin and inflammation—a key advantage during menopause when energy expenditure drops and visceral fat increases.

For menopausal women in particular, Metabolic Balance® offers tailored nutrition that directly addresses hormonal and metabolic shifts characteristic of this life stage and for the individual person as no 2 plans are the same. Hormonal decline during menopause often leads to increased abdominal fat, insulin resistance, elevated cholesterol, and blood pressure—all components of metabolic syndrome. (7,8)

By formulating individualized plans that balance macronutrients, emphasize fiber-rich whole foods, and stabilize blood sugar, the program mitigates these risks. Anecdotal reports and clinician feedback in Germany indicate up to 70% of menopausal participants reduce or eliminate medications as their symptoms (e.g., hot flashes, fatigue, low libido) improve through dietary change alone. This evidence-backed, hormone-sensitive method makes Metabolic Balance® a powerful tool for women seeking metabolic and symptom relief during menopause.

If you want to find out more please click here or book with one of our metabolic balance coaches for a free discovery call to find out more and see if this is the right fit for you.

Best Exercise for Perimenopause and Menopause Woman

Despite your best efforts to reduce calories, implement extra workouts and avoiding junk food that weight just keeps piling on! But you might find that it is not just how often or how long you work out but also the type of exercise that you do that needs to change, so switching your workouts might be just the thing.

Resistance Training & Strength-Building

Weightlifting, bodyweight training, and using weighted vests—even during daily chores is highly recommended to preserve lean muscle and bone density, which for menopause woman becomes much harder as their estrogen and testosterone start to drop and insulin and inflammation starts to climb.

Cardiovascular and Zone-2 Exercise

Zone 2 training is a type of cardiovascular exercise performed at a specific heart rate intensity that primarily targets your aerobic system—where your body efficiently burns fat for fuel. It’s often referred to as the “fat-burning zone” or the “aerobic base” zone.

Zone-2 training supports mitochondrial health and cardiovascular resilience—a key pillar of her holistic approach.  Zone 2 is for building health span—not just lifespan. In menopause, where inflammation, insulin resistance, and fatigue can increase, zone 2 training offers a low-stress, high-impact strategy for staying metabolically fit and energized.

 

Definition of Zone 2

Zone 2 corresponds to about 60–70% of your maximum heart rate (MHR). At this intensity:

• Your breathing is elevated but you can still hold a conversation (also called the “talk test”).
• You primarily use fat as a fuel source, not glycogen (sugar).
• You increase mitochondrial density and efficiency, improving endurance and metabolic health.
• Duration: 30–90 minutes for optimal benefit, though 20 mins is a good start.

 

Why Zone 2 Training Matters—Especially in Midlife & Menopause

• Zone 2 training supports metabolic flexibility (switching between fat and sugar for energy).
• It improves insulin sensitivity and reduces the risk of type 2 diabetes.
• It supports mitochondrial health, crucial for energy, longevity, and reducing fatigue.
• It may help reduce visceral fat, the dangerous fat around organs that often increases during menopause.
• It enhances recovery and reduces chronic stress load compared to high-intensity training.

 

How to Calculate Your Zone 2 Heart Rate

A general formula:

Zone 2 HR = (220 – your age) × 0.6 to 0.7

So, if you’re 50:

MHR = 220 – 50 = 170

Zone 2 = 102 to 119 bpm

Alternatively, for a more accurate method, especially for trained individuals, many use lactate threshold tests or VO₂ max assessments through labs or wearables (like Garmin, Whoop, or Apple Watch with HR tracking).

 

What are the Best Zone 2 Activities to do for Menopause

• Brisk walking
• Light jogging
• Cycling at a moderate pace
• Rowing machine at a steady pace
• Hiking on flat terrain
• Swimming laps at moderate pace

 

How Zone 2 Training Differs from Other Zones

Zone	% Max HR	Fuel Source	Benefit
1	50–60%	Fat	Recovery, low intensity
🟢2	60–70%	Mostly fat	Aerobic capacity, fat-burning
3	70–80%	Fat & carbs	Higher endurance, some stress load
4	80–90%	Mostly carbs	Anaerobic, lactate tolerance
5	90–100%	Carbs (glycogen)	Peak power, VO₂ max, short bursts

 

What are the Worst Exercises for Perimenopause and Menopause woman

High intensity training

• Increases cortisol, which can worsen belly fat and sleep problems.
• Can deplete progesterone and DHEA when stress is high.
• Promotes muscle loss if not balanced with strength training and proper recovery.

Note: Overtraining is a common cause of persistent fatigue and plateaued weight loss in menopausal women.

Long Distance Running

• Promotes oxidative stress and inflammation.
• Can worsen joint pain, pelvic floor strain, and bone loss if not paired with resistance work.
• Not effective for preserving muscle mass.

Conclusion

Menopause isn’t a sentence to sleepless nights, pain, muffin tops and mood swings —it’s a transition with choices. Menopause is a complex biological transition with widespread effects on women’s bodies and lives. A multi-dimensional approach centered on evidence-based hormone therapy, a nutrient-dense anti-inflammatory diet, appropriate movement/exercise, and mind-body approaches are all key in helping woman navigate this and enable them to live the second half of their life being healthier, richer, and more vibrant than ever before.

 

References:

1. Lovejoy, J. C., Champagne, C. M., de Jonge, L., Xie, H., & Smith, S. R. (2008). Increased visceral fat and decreased energy expenditure during the menopausal transition. International Journal of Obesity, 32(6), 949–958. https://doi.org/10.1038/ijo.2008.25
2. Carr, M. C. (2003). The emergence of the metabolic syndrome with menopause. The Journal of Clinical Endocrinology & Metabolism, 88(6), 2404–2411. https://doi.org/10.1210/jc.2003-030242
3. Fung, T. T., McCullough, M. L., Newby, P. K., Manson, J. E., Meigs, J. B., Rifai, N., … & Hu, F. B. (2005). Diet-quality scores and plasma concentrations of markers of inflammation and endothelial dysfunction. The American Journal of Clinical Nutrition, 82(1), 163–173. https://doi.org/10.1093/ajcn.82.1.163
4. Matthews, K. A., Crawford, S. L., Chae, C. U., Everson-Rose, S. A., Sowers, M. F., Sternfeld, B., & Sutton-Tyrrell, K. (2009). Are changes in cardiovascular disease risk factors in midlife women due to chronological aging or to the menopausal transition? Journal of the American College of Cardiology, 54(25), 2366–2373. https://doi.org/10.1016/j.jacc.2009.10.009
5. Anton, S. D., Moehl, K., Donahoo, W. T., Marosi, K., Lee, S. A., Mainous, A. G., … & Mattson, M. P. (2018). Flipping the metabolic switch: Understanding and applying the health benefits of fasting. Obesity, 26(2), 254–268. https://doi.org/10.1002/oby.22065
6. Meffert, Cornelia; Gerdes, Nikolaus: Program Adherence and Effectiveness of a Commercial Nutrition Program: The Metabolic Balance Study. Journal of Nutrition and Metabolism, Volume 2010 (2010), Article ID 197656;  (http://www.hindawi.com/journals/jnume/2010/197656.html)
7. P. R. Thomas, Ed., Committee to Develop Criteria for Evaluating the Outcomes of Approaches to Prevent and Treat Obesity and Institute of Medicine: Weighing the Options: Criteria for Evaluating Weight-Management Programs, National Academies Press, Washington, DC, USA, 1995
8. Hauner H, Wechsler JG, Kluthe R et al: Qualitätskriterien für ambulante Adipositasprogramme [Quality criteria for outpatient obesity programs],  Akt. Ernaehr. Med. 25 (2000), 163-165