Although DUTCH testing is commonly used in women’s health, it can also provide valuable insight into men’s hormone health. If you are a provider who is used to running DUTCH tests on women, or anyone who is curious about using this panel in men, this article is for you. A DUTCH test is a comprehensive hormone panel that evaluates androgen and estrogen patterns alongside HPA axis function and select organic acid markers. This helps to put symptoms such as fatigue, low libido, poor sleep, weight gain, and metabolic dysfunction into a broader endocrine context in both men and women.  

For providers newer to male hormone testing, the key is not to interpret each hormone in isolation. Testosterone, estrogen, metabolic health, sleep, and stress physiology often influence one another. 

Meet Ryan

Ryan is 38 and has been trying to conceive with his wife for over one year. His wife is an established patient, and her provider recommended evaluating Ryan as part of their fertility work-up. 

Ryan has prediabetes, metabolic syndrome, a BMI of 30.1, and gradual weight gain over three years. He also reports poor sleep, fatigue, low mood, and low libido. Recent labs showed fasting glucose of 112 mg/dL, triglycerides of 200 mg/dL, LDL of 160 mg/dL, and HDL of 35 mg/dL. His semen analysis is pending. 

A typical male fertility evaluation begins with a reproductive history and semen analysis. When symptoms or findings suggest a hormonal contribution, additional testing may include morning serum testosterone, FSH, LH, prolactin, SHBG, and free testosterone. The DUTCH test provides additional detail on hormone metabolism, cortisol production and clearance, and organic acid markers that can provide further insight into reproductive health. 

DUTCH Complete Hormone Testing Summary 

Let’s assess Ryan’s results using the DUTCH Dozen Framework. 

Androgen Assessment 

Ryan has normal total DHEA production but low testosterone and low-end 5a-androstanediol for his age. 

DHEA is produced primarily by the adrenal glands, while approximately 95% of testosterone production occurs in the testes. This means a man can have normal adrenal androgen production while still having inadequate testicular testosterone production. 

Clinical Pearl: The majority of testosterone production occurs in the testes, not the adrenal glands. DHEA levels reflect adrenal health, while testosterone levels reflect gonadal and metabolic health.  

Low testosterone may contribute to Ryan’s low libido, low mood, fatigue, and difficulty maintaining healthy body composition. In Ryan’s case, the low-end result suggests that tissue androgen levels may also be lower than ideal.  

5a-androstanediol is a downstream metabolite of DHT and can provide insight into 5a-reductase activity and intracellular androgen activity, or tissue androgen levels. 5a-reductase metabolites like 5a-androstanediol are made out the target tissues, where you want the androgens working. The 5a-androstanediol is a good marker for understanding how testosterone is working in his body. 5b-reductase is almost exclusively a liver detox enzyme; 5b metabolites can help us identify androgen production and liver detox. The 5a-metabolism slider looks at the balance between the two, helping identify where his androgens are being used regardless of levels. 

Ryan’s low-end 5a-androstanediol suggests relatively low tissue androgen activity, even though his overall balance between the 5a and 5b pathways is normal. 

On the DUTCH Test, urinary testosterone reflects bioavailable testosterone and is most closely related to free testosterone in serum. Because urinary hormone testing does not replace the conventional evaluation of hypogonadism, serum testing should also be considered.  

Fertility concerns also change the treatment approach. Exogenous testosterone therapy suppresses LH and FSH signaling and can significantly reduce sperm production.¹

Clinical Pearl: Exogenous testosterone can suppress spermatogenesis. TRT should be avoided in men trying to conceive. 

Estrogen Assessment 

Ryan has elevated estradiol and estrone relative to his low testosterone. His 2-OH/4-OH ratio is low while his 2-OH/16-OH ratio and Phase 2 methylation activity are normal. 

Estrogen is essential for normal male physiology. Estradiol plays key roles in male reproductive health, HPG axis function, sexual function and libido, brain, bone, metabolic, and cardiovascular health. Most circulating estradiol in men is produced through peripheral aromatization of androgens, predominately within adipose tissue. 

In Ryan’s case, excess adiposity, prediabetes, and metabolic dysfunction may be contributing to greater aromatization and a relative shift from testosterone toward estrogen. Higher estradiol can also increase negative feedback on the hypothalamus and pituitary, potentially lowering testicular testosterone production.^2,3

Estradiol also supports spermatogenesis and sperm maturation, so estrogen should not simply be viewed as something to lower in men. Disrupted estrogen-androgen balance and the metabolic factors driving it may contribute to impaired reproductive function.⁴

Clinical Pearl: Estrogen isn’t just a “female hormone.” Men need estradiol for optimal health and normal physiologic function. When estrogen is elevated relative to testosterone, consider potential contributors such as excess adiposity, insulin resistance, and increased aromatase activity. 

Ryan’s 2-OH/16-OH ratio is normal, while his low 2-OH/4-OH ratio reflects a greater relative preference for the 4-OH pathway. 4-hydroxy estrogens can form reactive quinones and contribute to oxidative stress and DNA damage.⁵ This can have negative impacts on prostate health and potentially impair male fertility. 

Clinical Pearl: Just like in women, 4-OH-E1 is considered a genotoxic metabolite in men. Systemic inflammation can increase the 4-OH pathway. 

Cortisol Assessment 

Ryan’s overall diurnal cortisol pattern is normal, although his dinnertime free cortisol is elevated. His 24-hour free cortisol is within range, while metabolized cortisol is elevated and his cortisol clearance rate is borderline high. 

This pattern suggests that Ryan produced a relatively high amount of cortisol that day but also cleared it (converted the active cortisol into inactive metabolites) fairly quickly. Looking only at free cortisol could therefore underestimate his overall cortisol production. 

Clinical Pearl: Normal 24-hour free cortisol does not always mean cortisol production is normal. Elevated metabolized cortisol can indicate higher cortisol output, and metabolic dysfunction itself may contribute to increased cortisol clearance. 

Faster cortisol clearance is commonly seen with metabolic dysfunction, including obesity and impaired insulin resistance. Increased cortisol output may also worsen blood sugar regulation and visceral adiposity.⁶ Higher cortisol output is relevant to male hormone health because chronic HPA-axis activation can suppress HPG-axis signaling and contribute to lower testosterone production.⁷

Organic Acids Assessment 

Ryan’s organic acid results show elevated quinolinate and low waking melatonin. Elevated quinolinate reflects increased inflammatory activity and fits with his broader picture of metabolic dysfunction and oxidative stress.⁸

Low waking melatonin is also notable given his difficulty falling asleep and waking unrefreshed. Poor sleep can negatively affect testosterone production, insulin sensitivity, metabolic health, and reproductive function.⁹

Clinical Pearl: Sleep is an important part of male hormone health. Testosterone production is closely tied to sleep, so inadequate or disrupted sleep can contribute to lower testosterone and may also negatively affect fertility. 

Putting It All Together 

Ryan’s results are best understood as an interconnected pattern rather than isolated abnormal values. 

His excess adiposity, prediabetes, and metabolic dysfunction are consistent with impaired insulin sensitivity and may be contributing to lower testosterone production and greater aromatization to estrogen. Metabolic dysfunction may also contribute to faster cortisol clearance, while higher cortisol output can further worsen blood sugar regulation and visceral adiposity. 

Poor sleep and chronic HPA-axis activation can further disrupt HPG-axis signaling and testosterone production. Together, these factors can create a self-reinforcing cycle. 

For Ryan, the goal is not simply to raise testosterone or lower estrogen. Treatment should focus on contributing factors, including metabolic health, excess adiposity, sleep, stress, and inflammation. 

Treatment Considerations 

Based on Ryan's DUTCH test findings and metabolic concerns, additional serum evaluation may include fasting insulin, HbA1c, and hs-CRP. Given his excess weight, poor sleep, and waking unrefreshed, screening for obstructive sleep apnea should be considered. 

Lifestyle-driven weight loss is considered first-line therapy when low testosterone occurs with obesity and another underlying cause has not been identified.¹⁰ For Ryan, priorities include a whole-food, Mediterranean-style diet emphasizing vegetables, fruit, quality protein, fiber, omega-3 fatty acids, and antioxidant-rich foods while limiting added sugar, ultra-processed foods, and excess alcohol. 

Exercise should include resistance training at least twice weekly, targeting all major muscle groups, along with at least 150 minutes of moderate-intensity aerobic activity per week and regular daily movement.¹¹ Improving sleep and reducing chronic stress are also important. 

Targeted supplementation may provide additional support, but supplements should remain secondary to the lifestyle changes. Supplemental options could include berberine for metabolic support, ashwagandha for stress and HPA-axis support, sulforaphane for antioxidant and Phase II estrogen-metabolism support, or melatonin for sleep and antioxidant support. 

Registered DUTCH providers can refer to the DUTCH Treatment Guide for additional ideas related to low testosterone in males (pp. 18–19), high estrogen in males (pp. 14–15), 4-OH estrogen metabolism preference (p. 28), high cortisol (p. 40), anti-inflammatory support (p. 53), and insulin resistance support (p. 54). 

Would Ryan be a good candidate for GLP-1 therapy? 

GLP-1 receptor agonists are not currently approved as treatments for male hypogonadism or infertility. However, in men like Ryan with obesity and metabolic dysfunction, anti-obesity pharmacotherapy may be considered for the underlying metabolic condition.  

Emerging research suggests GLP-1 receptor agonist-associated weight loss may also improve testosterone and potentially some semen parameters in men with obesity or functional hypogonadism, although more research is needed before these medications can be considered fertility therapies.¹²

Because Ryan is actively trying to conceive, exogenous testosterone therapy should be avoided. If testosterone remains low after addressing reversible contributors, referral for fertility-preserving treatment options such as hCG, SERMs, or aromatase inhibitors may be appropriate.¹

When Should You Reassess? 

Hormonal and fertility improvements take time. Reassessment at approximately three months allows time for a new cycle of spermatogenesis and is a reasonable interval for repeating semen analysis after meaningful lifestyle or treatment changes. Some semen parameters may improve sooner. In one randomized trial, eight weeks of diet-induced weight loss in men with obesity significantly improved sperm concentration and total sperm count, and improvements were maintained in men who maintained the weight loss.¹³ 

Testosterone can also improve as metabolic health and body composition improve. Rather than focusing on a fixed timeline, the magnitude and sustainability of weight loss appear to be important predictors of testosterone recovery. Even weight loss of approximately 5% may significantly increase testosterone in men with obesity, with greater weight loss generally associated with larger improvements.^3,10

For Ryan, reassessing symptoms, metabolic markers, hormones, and fertility parameters after approximately three months can help determine whether the initial plan is moving him in the right direction. 

Summary 

Male hormone health is rarely about testosterone alone. Ryan’s low testosterone, elevated estrogens, increased cortisol production, poor sleep, and metabolic dysfunction appear to be part of a larger interconnected pattern. 

A DUTCH Test for men can help providers see these relationships and identify potential contributing factors that may be missed when individual hormones are viewed in isolation. Look at hormone relationships, consider the metabolic and lifestyle context, and focus treatment on the factors driving the pattern. 

For Ryan, improving metabolic health, sleep, stress physiology, and body composition may support healthier hormone balance and overall reproductive health. 

References 

1. Schlegel PN, Sigman M, Collura B, et al. Diagnosis and treatment of infertility in men: AUA/ASRM guideline part II. Fertil Steril. 2021;115(1):62-69. doi:10.1016/j.fertnstert.2020.11.016. 
2. Raven G, de Jong FH, Kaufman JM, de Ronde W. In men, peripheral estradiol levels directly reflect the action of estrogens at the hypothalamo-pituitary level to inhibit gonadotropin secretion. J Clin Endocrinol Metab. 2006;91(9):3324-3328. doi:10.1210/jc.2006-0462. 
3. Wittert G, Grossmann M. Obesity, type 2 diabetes, and testosterone in ageing men. Rev Endocr Metab Disord. 2022;23(6):1233-1242. doi:10.1007/s11154-022-09746-5. 
4. Schulster M, Bernie AM, Ramasamy R. The role of estradiol in male reproductive function. Asian J Androl. 2016;18(3):435-440. doi:10.4103/1008-682X.173932. 
5. Cavalieri EL, Rogan EG. Unbalanced metabolism of endogenous estrogens in the etiology and prevention of human cancer. J Steroid Biochem Mol Biol. 2011;125(3-5):169-180. doi:10.1016/j.jsbmb.2011.03.008 
6. Holt HB, Wild SH, Postle AD, et al. Cortisol clearance and associations with insulin sensitivity, body fat and fatty liver in middle-aged men. Diabetologia. 2007;50(5):1024-1032. doi:10.1007/s00125-007-0629-9. 
7. Pintana, H., Chattipakorn, N. & Chattipakorn, S. Testosterone deficiency, insulin-resistant obesity and cognitive function . Metab Brain Dis 30, 853–876 (2015). https://doi.org/10.1007/s11011-015-9655-3 
8. Lugo-Huitrón R, Ugalde Muñiz P, Pineda B, Pedraza-Chaverrí J, Ríos C, Pérez-de la Cruz V. Quinolinic acid: an endogenous neurotoxin with multiple targets. Oxid Med Cell Longev. 2013;2013:104024. doi:10.1155/2013/104024 
9. Su L, Zhang SZ, Zhu J, Wu J, Jiao YZ. Effect of partial and total sleep deprivation on serum testosterone in healthy males: A systematic review and meta-analysis. Sleep Med. 2021;88:267-273. doi:10.1016/j.sleep.2021.10.031. 
10. Anawalt BD, O’Connor KM, Grossmann M. Adult male hypogonadism: A review. JAMA. 2026;335(24):2146-2159. doi:10.1001/jama.2026.8526. 
11. U.S. Department of Health and Human Services. Physical Activity Guidelines for Americans. 2nd ed. Washington, DC: U.S. Department of Health and Human Services; 2018. 
12. Ghassab Deameh M, Ramez M, Rowaiee R, et al. Effects of glucagon-like peptide-1 receptor agonists on male reproductive hormones, semen parameters, and metabolic outcomes: A systematic review. J Sex Med. 2026;23(2). doi:10.1093/jsxmed/qdaf381. 
13. Andersen E, Juhl CR, Kjøller ET, et al. Sperm count is increased by diet-induced weight loss and maintained by exercise or GLP-1 analogue treatment: A randomized controlled trial. Hum Reprod. 2022;37(7):1414-1422. doi:10.1093/humrep/deac096.