Systematic Review

Dietary Interventions and Testosterone Levels in Obese

Men: A Systematic Review Comparing the Mediterranean Diet,
Ketogenic Diet, and Intermittent Fasting
Sandro La Vignera * and Rosita A. Condorelli

Department of Clinical and Experimental Medicine, University of Catania, Via S. Sofia 78, 95123 Catania, Italy;
[Link]@[Link]
* Correspondence: sandrolavignera@[Link]

Abstract
Background/Objectives: Male obesity secondary hypogonadism (MOSH) is a highly
prevalent condition characterised by reduced testosterone levels in obese men, driven
by increased aromatase activity, reduced SHBG, insulin resistance, and HPG axis suppres-
sion. Dietary interventions represent a cornerstone of non-pharmacological management;
however, the comparative efficacy of different dietary patterns on testosterone restora-
tion remains unclear. Methods: We conducted a systematic literature review following
PRISMA 2020 guidelines. Comprehensive searches were performed in SciSpace, Google
Scholar, and PubMed through June 2026. Eligible studies included human adult males
with obesity (BMI ≥ 30 kg/m2 ) undergoing Mediterranean diet (MedDiet), ketogenic diet
(KD/VLCKD), or intermittent fasting (IF) interventions, with quantitative assessment of
testosterone or androgen status. Results: From 697 initial records, 500 unique papers
were identified after deduplication. Following abstract screening (n = 442 excluded) and
full-text assessment (n = 6 excluded), 52 studies were included in the final synthesis. VL-
CKD demonstrated the most consistent evidence for testosterone improvement, with RCTs
reporting significant increases in total testosterone (+1.5 to +3.0 nmol/L). Intermittent
fasting showed promising but more heterogeneous results. Evidence for Mediterranean
diet was limited, focusing primarily on metabolic rather than hormonal outcomes. Weight
loss emerged as a critical mediator across all dietary interventions (~3 nmol/L per 10 kg
weight loss). Conclusions: Among dietary interventions for MOSH, VLCKD shows the
strongest evidence for testosterone restoration in obese men, through rapid weight loss,
improved insulin sensitivity, reduced inflammation, and potential direct HPG axis effects.
Intermittent fasting represents a viable alternative. Mediterranean diet, while beneficial for
cardiovascular health, lacks robust interventional evidence for testosterone improvement
in this population. Systematic Review Registration: This review was not prospectively
registered. PROSPERO registration is recommended for future updates.
Academic Editors: Feng Jiang, Yuhui
Ruan and Yilang Tang Keywords: obesity; testosterone; hypogonadism; ketogenic diet; Mediterranean diet;
Received: 28 June 2026 intermittent fasting; male obesity secondary hypogonadism; VLCKD; androgens; dietary
Revised: 20 July 2026 intervention
Accepted: 22 July 2026
Published: 24 July 2026
Copyright: © 2026 by the authors.
Licensee MDPI, Basel, Switzerland. 1. Introduction
This article is an open access article
distributed under the terms and
Male obesity secondary hypogonadism (MOSH), also termed functional hypogo-
conditions of the Creative Commons nadism, represents one of the most prevalent endocrine disorders among men with excess
Attribution (CC BY) license. adiposity [1,2]. Epidemiological data consistently demonstrate an inverse relationship

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Nutrients 2026, 18, 2417 2 of 14

between body mass index (BMI) and serum testosterone concentrations, with obese men
exhibiting total testosterone levels 25–30% lower than their lean counterparts [3,4]. The
clinical consequences of this hormonal deficit extend beyond reproductive dysfunction
and encompass metabolic dysregulation, cardiovascular risk, impaired quality of life, and
psychological morbidity [5,6].
The pathophysiology of MOSH is multifactorial and bidirectional. Adipose tissue
hypertrophy increases the expression and activity of aromatase (CYP19A1), the enzyme re-
sponsible for peripheral conversion of testosterone to oestradiol, thereby creating a negative
feedback loop that suppresses gonadotropin-releasing hormone (GnRH) pulsatility and,
consequently, luteinising hormone (LH) secretion [7,8]. Concurrently, obesity-associated
hyperinsulinaemia and insulin resistance reduce hepatic synthesis of sex hormone-binding
globulin (SHBG), further diminishing bioavailable testosterone fractions [9]. Systemic
low-grade inflammation—characterised by elevated IL-6, TNF-α, and CRP—exerts direct
inhibitory effects on Leydig cell steroidogenesis [10,11]. The ‘Gut Endotoxin Leading to
a Decline IN Gonadal function’ (GELDING) theory has been proposed as an additional
mechanistic pathway, suggesting that obesity-induced intestinal dysbiosis and lipopolysac-
charide (LPS) translocation may compromise testicular function [12]; however, direct causal
evidence in humans remains limited, and this mechanism warrants further prospective
investigation before definitive conclusions can be drawn.
Given the reversible nature of MOSH—in contrast to organic hypogonadism—lifestyle
interventions, particularly dietary modifications, represent the primary therapeutic strat-
egy before considering testosterone replacement therapy (TRT) [13,14]. Weight loss of
5–10% of body weight has been associated with clinically meaningful testosterone incre-
ments, and the magnitude of hormonal recovery appears proportional to the degree of
weight reduction [15,16]. However, the optimal dietary approach to maximise testosterone
restoration in obese men remains undefined.
Three dietary strategies have received particular attention in this context: (1) the
Mediterranean diet (MedDiet), characterised by high consumption of plant foods, olive
oil, moderate fish and poultry intake, and low red meat consumption, with established
cardioprotective and anti-inflammatory properties [17,18]; (2) the ketogenic diet (KD)
and its clinical variant, the very-low-calorie ketogenic diet (VLCKD), defined by severe
carbohydrate restriction (<50 g/day) leading to nutritional ketosis, with demonstrated
efficacy in rapid weight loss and metabolic improvement [19,20]; and (3) intermittent
fasting (IF), encompassing various time-restricted eating (TRE) and alternate-day fasting
(ADF) protocols [21,22]. These three dietary strategies were selected for synthesis on the
basis of the volume of available evidence, their contrasting metabolic mechanisms, their
established clinical relevance in obesity management, and their growing adoption in clinical
and research settings, enabling a meaningful comparative synthesis.
Despite a growing body of literature on each of these dietary patterns individually, no
systematic review has directly compared their relative efficacy in improving testosterone
levels specifically in obese men. The rising global prevalence of male obesity, the growing
recognition of MOSH as a distinct and clinically relevant entity, and increasing interest
in dietary alternatives to testosterone replacement therapy (TRT) collectively underline
the importance and timeliness of such a synthesis. This systematic review aims to fill
this evidence gap by synthesising available data, evaluating the hormonal and metabolic
outcomes of MedDiet, KD/VLCKD, and IF interventions, and providing evidence-informed
recommendations for clinical practice.

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2. Materials and Methods

2.1. PRISMA 2020 Compliance Statement
This systematic review was conducted and reported in accordance with the Preferred
Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 statement [23].
The completed PRISMA 2020 checklist is provided as Supplementary Material S6 (Table S6).

2.2. Protocol and Registration

This review was not prospectively registered. The authors acknowledge that prospec-
tive registration in PROSPERO ([Link] accessed on
20 June 2026) represents a fundamental requirement of methodological rigour for sys-
tematic reviews, and the absence of registration constitutes a significant methodological
limitation of the present work. Retrospective registration was not pursued following
completion of the review. The authors are committed to prospective registration in PROS-
PERO for any future updates of this review or for related systematic reviews conducted in
this field.

2.3. Eligibility Criteria

Studies were eligible for inclusion if they met the following PICO criteria:
• Population (P): Adult males (age ≥ 18 years) with obesity (BMI ≥ 30 kg/m2 ) or
overweight with metabolic complications.
• Intervention (I): Mediterranean diet, ketogenic diet (including VLCKD, LCHF), or
intermittent fasting (TRE, ADF, 5:2 diet, Ramadan fasting).
• Comparison (C): Control diet, standard hypocaloric diet, or comparison between the
three dietary patterns.
• Outcome (O): Primary: serum total testosterone (nmol/L or ng/dL). Secondary: free
testosterone, SHBG, LH, FSH, oestradiol, body weight, BMI, HOMA-IR, lipid profile,
inflammatory markers.
Eligible study designs included RCTs, non-randomised controlled trials, prospective
and retrospective cohort studies, cross-sectional studies, systematic reviews, and meta-
analyses. Animal studies were included only if they provided mechanistic insights not
available from human studies.

2.4. Information Sources and Search Strategy

Systematic searches were conducted in SciSpace, Google Scholar, and PubMed from
database inception through June 2026. These three databases were selected to provide
broad indexing coverage across biomedical, nutritional, and interdisciplinary literature.
No publication year restrictions were applied. The search strategy combined controlled
vocabulary (MeSH terms in PubMed) with free-text terms. The complete search strings are
reported in Supplementary Material S1 (Table S1). The absence of additional databases,
including EMBASE, Web of Science, the Cochrane Library, and Scopus, is acknowledged as
a potential limitation of the search strategy and is further discussed in Section 4.2.
PubMed primary search string: (“Diet, Mediterranean”[MeSH Terms] OR “Diet,
Ketogenic”[MeSH Terms] OR “Fasting”[MeSH Terms] OR “Caloric Restriction”[MeSH
Terms] OR “Diet, Carbohydrate-Restricted”[MeSH Terms] OR very low calorie ketogenic
diet[Title/Abstract] OR VLCKD[Title/Abstract] OR alternate day fasting[Title/Abstract]
OR time-restricted eating[Title/Abstract]) AND (“Testosterone”[MeSH Terms] OR “An-
drogens”[MeSH Terms] OR free testosterone[Title/Abstract] OR “Hypogonadism”[MeSH
Terms]) AND (“Obesity”[MeSH Terms] OR “Overweight”[MeSH Terms] OR “Weight
Loss”[MeSH Terms]) AND “Male”[MeSH Terms]

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2.5. Study Selection

All identified records were imported into a reference management system and dedu-
plicated. Two independent reviewers (S.L.V. and R.A.C.) screened titles and abstracts
against the eligibility criteria. Full texts of potentially eligible studies were retrieved and
assessed independently. Disagreements were resolved by consensus. The selection process
is illustrated in the PRISMA 2020 flow diagram (Figure 1).

Figure 1. PRISMA 2020 flow diagram illustrating the systematic search and study selection process
for the review of dietary interventions and testosterone levels in obese men.

2.6. Data Extraction

Data were extracted by one reviewer and verified by a second using a standardised
extraction form. Variables collected included: first author, year, country, study design,
sample size, participant characteristics (age, BMI, baseline testosterone), intervention
description (dietary pattern, duration, caloric target), comparator, follow-up duration,
primary and secondary outcomes, and risk of bias assessment. The complete data extraction
form is provided in Supplementary Material S2 (Table S2).

2.7. Risk of Bias Assessment

Risk of bias in RCTs was assessed using the Cochrane Risk of Bias 2 (RoB 2) tool. Non-
randomised studies were evaluated using the Newcastle–Ottawa Scale (NOS). Systematic
reviews were appraised using the AMSTAR-2 checklist. Detailed risk of bias results are
presented in Supplementary Materials S3–S5 (Tables S3–S5). Overall, risk of bias across
included RCTs ranged from low to some concerns; the most common source of bias was
the absence of participant and personnel blinding, which is inherent to dietary intervention
trials. The majority of observational studies assessed using the Newcastle–Ottawa Scale
achieved scores of ≥6, indicating moderate to good quality.

2.8. Data Synthesis

Due to the heterogeneity of dietary interventions, study populations, and outcome
reporting, a narrative synthesis was performed. Where sufficient quantitative data were
available from comparable studies, effect estimates were summarised descriptively. Sub-
group analyses were conducted by dietary pattern (MedDiet vs. KD/VLCKD vs. IF), study
design, and intervention duration.

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3. Results
3.1. Study Selection
The database searches retrieved 697 records in total (SciSpace: ~200; Google Scholar:
~250; PubMed: 247). After deduplication, 500 unique records were screened at the title and
abstract level. Following abstract screening, 442 records were excluded for not meeting
eligibility criteria. Full texts of 58 records were assessed for eligibility, of which 6 were
excluded (reasons: 3 did not report testosterone outcomes; 2 included exclusively female
participants; 1 was a conference abstract without full-text data). Fifty-two studies were in-
cluded in the final qualitative synthesis. The complete study selection process is illustrated
in the PRISMA 2020 flow diagram (Figure 1).

3.2. Characteristics of Included Studies

The 52 included studies comprised: 18 RCTs, 12 prospective cohort studies, 8 sys-
tematic reviews or meta-analyses, 7 retrospective or cross-sectional studies, and 7 animal
experimental studies providing mechanistic data. Publication years ranged from 1985 to
2026. Studies were conducted across Europe (n = 24), North America (n = 14), Asia (n = 8),
and other regions (n = 6). Sample sizes in human studies ranged from 12 to 511 participants
(median 64 males). Mean baseline BMI ranged from 30.1 to 48.6 kg/m2 , and mean baseline
total testosterone ranged from 7.2 to 14.8 nmol/L, confirming a hypogonadal or low-normal
hormonal profile at enrolment.

3.3. Very-Low-Calorie Ketogenic Diet (VLCKD) and Testosterone

VLCKD emerged as the dietary intervention with the strongest currently available
evidence for testosterone improvement in obese men, though the overall certainty of
this evidence remains moderate, limited by study heterogeneity, relatively small sample
sizes, and variable follow-up durations. Across the included RCTs and cohort studies,
multiple studies reported statistically significant increases in total testosterone following
VLCKD, with changes ranging from +1.5 to +3.0 nmol/L from baseline [24–26]. In a
landmark RCT comparing VLCKD to a standard hypocaloric diet, VLCKD-treated men
demonstrated significantly greater testosterone increments at 12 weeks (∆ + 2.4 nmol/L
vs. ∆ + 1.1 nmol/L; p < 0.05), independent of the degree of weight loss achieved [27]. Free
testosterone and SHBG also improved significantly in most VLCKD studies [28,29].
The testosterone-raising effect of VLCKD appears to be mediated through multiple
pathways. First, rapid and substantial weight loss (typically 8–15 kg over 8–12 weeks)
reduces adipose aromatase activity and restores HPG axis sensitivity [30]. Second, the
marked improvement in insulin sensitivity—reflected by reductions in fasting insulin
(mean −40–60%) and HOMA-IR—reduces hyperinsulinaemia-driven SHBG suppression,
thereby increasing bioavailable testosterone fractions [31,32]. Third, VLCKD exerts potent
anti-inflammatory effects, with significant reductions in IL-6, TNF-α, and CRP, relieving
inflammatory inhibition of Leydig cell steroidogenesis [33,34].
Several studies documented improvements in LH pulsatility and amplitude following
VLCKD, suggesting partial restoration of HPG axis function beyond the peripheral aro-
matase effect alone [16]. Benefits were observed as early as 4–8 weeks into VLCKD, with
maximum testosterone increments typically achieved at 12–16 weeks corresponding to the
nadir of weight loss [35].

3.4. Intermittent Fasting (IF) and Testosterone

Intermittent fasting encompasses heterogeneous protocols, and the evidence for testos-
terone improvement, while promising, is more variable than for VLCKD. Studies employing
16:8 or 18:6 TRE protocols in obese men reported modest but consistent improvements in

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total testosterone (+0.8 to +1.6 nmol/L) alongside reductions in body weight (−3–7 kg) and
improvements in insulin sensitivity [36,37]. La Vignera and Condorelli [38] published a
comprehensive review specifically addressing IF effects on male reproductive hormones,
reporting that TRE protocols were associated with improvements in testosterone, LH, and
sperm parameters in overweight and obese men, with the magnitude of benefit correlating
with the degree of caloric restriction achieved.
The landmark ADF trial by Trepanowski et al. [35] demonstrated significant weight
loss (−6.5 kg at 24 weeks) and improvements in cardiometabolic risk factors in obese adults.
Hormonal outcomes, including SHBG and free androgen index (FAI), were not reported as
pre-specified endpoints in the Trepanowski et al. [35] cardioprotection trial; accordingly,
previously cited secondary hormonal analyses attributing specific SHBG and free testos-
terone improvements to this dataset are not directly supported by the published report
and have been corrected in the present revision. Studies on the 5:2 protocol and Ramadan
fasting demonstrated variable testosterone effects, with some studies reporting transient
decreases during acute fasting phases followed by recovery upon refeeding [39,40].
Preclinical data from high-fat-diet-fed male rodents consistently demonstrate that
IF protocols restore testosterone and LH levels, improve sperm quality, and upregulate
steroidogenic enzymes (StAR, CYP11A1, CYP17A1) in Leydig cells [41,42]. The SIRT-
1/NRF2/P38 MAPK/NLRP3 pathway has been identified as a key mechanistic link be-
tween IF-induced metabolic improvement and gonadal function restoration [43].

3.5. Mediterranean Diet (MedDiet) and Testosterone

The evidence base for MedDiet-specific testosterone effects in obese men is notably
more limited compared to VLCKD and IF. Cross-sectional studies consistently demonstrate
positive associations between MedDiet adherence scores and testosterone levels in adult
men [28,38]. A large European cohort study (n = 1759 men) reported that men in the highest
MedDiet adherence tertile had total testosterone levels 1.2–1.8 nmol/L higher than those in
the lowest tertile, after adjustment for BMI, age, and physical activity [12].
RCTs specifically testing MedDiet in obese men with MOSH as a primary outcome are
lacking. Most interventional studies on MedDiet have focused on cardiovascular, metabolic,
or erectile function outcomes, with testosterone assessed as a secondary or exploratory
variable. Where reported, MedDiet interventions of 12–24 weeks duration produced modest
testosterone improvements (+0.5 to +1.2 nmol/L) that did not consistently reach statistical
significance [38,44,45].
The MedDiet contains several bioactive components with theoretical androgenic
potential: olive oil polyphenols (oleuropein, hydroxytyrosol) with anti-inflammatory and
antioxidant properties; omega-3 fatty acids from fish and nuts modulating prostaglandin
synthesis and reducing IL-6 and TNF-α; and zinc-rich foods (legumes, nuts, seafood)
supporting testicular steroidogenesis [43,46,47]. A critical limitation is that MedDiet does
not produce the rapid and substantial weight loss achievable with VLCKD (typically
−2 to −5 kg vs. −8 to −15 kg over comparable periods), which appears to be a key driver
of testosterone restoration [48].

3.6. Comparative Analysis and Summary

Table 1 summarises the comparative testosterone outcomes across the three dietary pat-
terns. Weight loss emerged as a critical mediator across all interventions, with meta-analytic
data from bariatric surgery studies suggesting approximately 3 nmol/L testosterone in-
crease per 10 kg weight loss [16,41]. When dietary interventions are compared at equivalent
degrees of weight loss, hormonal benefits appear largely comparable, suggesting that the
magnitude of weight reduction—rather than specific macronutrient composition—is the

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primary determinant of testosterone recovery. However, VLCKD may confer additional

testosterone benefits beyond weight loss alone through: (1) direct reduction in insulin-
mediated SHBG suppression; (2) potential ketone body-mediated effects on hypothalamic
GnRH pulsatility; and (3) preferential reduction in visceral adipose tissue, the primary site
of aromatase activity [16,31,49].

Table 1. Summary of testosterone outcomes by dietary intervention in obese men.

Testosterone Baseline
Dietary Evidence Weight Loss Key Quality of Intervention
Change Testosterone
Intervention Level (kg) Mechanism Evidence Duration
(nmol/L) (nmol/L)
↓ Aromatase, ↑
RCTs, cohort SHBG, ↓
VLCKD +1.5 to +3.0 8–15 HIGH 8–24 weeks 8.5–11.2 nmol/L
studies Insulin, ↓
Inflammation
↓ Adiposity, ↑
Intermittent RCTs, cohort Insulin
+0.8 to +1.6 3–8 MODERATE 8–16 weeks 8.0–12.0 nmol/L
Fasting studies sensitivity, ↑
LH pulsatility
Anti-
Mediterranean Observational, inflammatory, LOW–
+0.5 to +1.2 2–5 12–52 weeks 9.0–13.0 nmol/L
Diet limited RCTs antioxidant MODERATE
components
↑ = increase; ↓ = decrease.

A visual summary of the comparative evidence, key mechanisms, and clinical recom-
mendation pathway is presented in Figure 2.

Figure 2. Visual summary of comparative evidence for dietary interventions on potential testosterone
restoration in male obesity secondary hypogonadism (MOSH). The figure illustrates testosterone
changes, weight loss, key mechanisms, and evidence quality for each dietary pattern, along with a
proposed clinical pathway for consideration (VLCKD for induction → IF as alternative → MedDiet
for long-term maintenance). This proposed pathway requires prospective validation in adequately
powered clinical trials before formal evidence-based endorsement. ↑ = increase; ↓ = decrease.

3.7. Safety and Tolerability

• VLCKD: The most commonly reported adverse effects include ‘keto-flu’ (fatigue,
headache, nausea) during the induction phase (weeks 1–2), constipation, and transient
LDL elevations. Hypoglycaemia risk in patients with type 2 diabetes requires careful

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medication adjustment. Long-term adherence beyond 12–16 weeks is challenging,

necessitating a structured dietary transition phase [19,20].
• Intermittent Fasting: Generally well-tolerated, with hunger and irritability during
fasting periods as the primary complaints. Concerns about muscle mass preservation
have not been confirmed when adequate protein intake is maintained. Not suitable
for patients with eating disorders or those on insulin/sulphonylurea therapy [21,22].
• Mediterranean Diet: The most favourable long-term safety profile, with no significant
adverse effects reported in clinical trials. High long-term adherence rates confer a
critical advantage for sustainable metabolic and hormonal benefits [17,18].

4. Discussion
This systematic review provides a comprehensive synthesis of evidence comparing
the effects of MedDiet, KD/VLCKD, and IF on testosterone levels in obese men. The
principal finding is that VLCKD demonstrates the greatest consistency of evidence for
testosterone restoration in this population, followed by IF, with MedDiet showing the most
limited evidence for direct hormonal improvement despite its well-established metabolic
and cardiovascular benefits. It is noted, however, that the overall certainty of evidence
across dietary patterns remains moderate, reflecting the heterogeneity of included studies,
variable follow-up durations, and differences in outcome reporting. Critically, it must be
emphasised that the outcomes reported across the majority of included studies are pre-
dominantly biochemical in nature—specifically changes in serum total or free testosterone
concentration—rather than the patient-important clinical endpoints that characterise symp-
tomatic hypogonadism. Evidence specifically addressing improvements in sexual function,
hypogonadal symptom burden (as assessed by validated symptom scores), body compo-
sition parameters (lean mass, fat mass), fertility indices (sperm concentration, motility,
morphology), and health-related quality of life as direct endpoints of dietary interven-
tion in MOSH is either absent or inconsistently reported across included studies. The
clinical significance of biochemical testosterone improvements observed in this review
therefore requires confirmation in future trials incorporating validated patient-relevant
clinical outcome measures.
It is essential to contextualise these findings within current endocrinological guide-
lines. Both the European Association of Andrology (EAA) and the European Society of
Endocrinology (ESE) position MOSH as a diagnosis of exclusion: before attributing hy-
pogonadism to obesity, clinicians must exclude primary and secondary organic causes
through a comprehensive diagnostic workup. This should include measurement of fasting
morning total testosterone on at least two separate occasions, together with assessment of
LH, FSH, and prolactin, and exclusion of pituitary or primary testicular pathology. Dietary
interventions should therefore be considered as part of an integrated management strategy
within this diagnostic framework, rather than as standalone treatments.
The greater evidence base for VLCKD in improving testosterone is consistent with its
distinctive metabolic profile. Unlike MedDiet or IF, VLCKD produces rapid and substantial
weight loss (often 8–15 kg over 8–12 weeks), driven by glycogen depletion, water loss,
and accelerated lipolysis. This rapid adiposity reduction translates directly into decreased
aromatase activity, reduced oestradiol production, and consequent disinhibition of the HPG
axis [7,8]. The simultaneous and marked improvement in insulin sensitivity—a hallmark
of VLCKD—addresses the SHBG suppression mechanism, further increasing bioavailable
testosterone fractions [9,31]. The relative contribution of weight loss per se versus the
specific metabolic effects of nutritional ketosis to observed testosterone improvements
remains uncertain, and this distinction warrants direct investigation in future trials.

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A critical methodological consideration relevant to interpreting these findings con-

cerns the measurement of testosterone fractions. In obesity, SHBG is suppressed by chronic
hyperinsulinaemia, such that total testosterone measurements may underestimate the
degree of hypogonadism. Conversely, with VLCKD-induced improvements in insulin
sensitivity, a rise in SHBG may partially attenuate the apparent increase in free testosterone,
despite a genuine improvement in androgenic status. Studies reporting only total testos-
terone may therefore underestimate the true benefit of dietary intervention. Future studies
should report both total testosterone and calculated free testosterone using the Vermeulen
equation, and SHBG measurement should be considered a co-primary outcome in clinical
trials of dietary intervention for MOSH.
The role of nutritional ketosis per se in testosterone regulation deserves particular
attention. Emerging evidence suggests that beta-hydroxybutyrate (BHB), the principal
circulating ketone body, may exert direct effects on hypothalamic GnRH neurones and
pituitary gonadotrophs beyond its metabolic effects [49]. Furthermore, the preferential
mobilisation of visceral adipose tissue during VLCKD may disproportionately reduce the
primary site of aromatase activity, explaining why VLCKD may confer testosterone benefits
exceeding those predicted by total weight loss alone [16].
Intermittent fasting’s hormonal effects are more heterogeneous, reflecting the diversity
of IF protocols and the variable caloric deficits achieved. The most consistent testosterone
benefits are observed with protocols producing meaningful weight loss (≥5% of body
weight), suggesting that IF’s androgenic effects are primarily weight loss-mediated rather
than fasting-specific. The comprehensive review by La Vignera and Condorelli [38] sup-
ports IF as a viable and evidence-based option for MOSH management, particularly for
patients who prefer dietary flexibility over macronutrient restriction.
The limited evidence for MedDiet-specific testosterone improvements reflects, in
part, the historical focus of MedDiet research on cardiovascular and metabolic rather than
reproductive endpoints. The cross-sectional associations between MedDiet adherence and
testosterone levels are consistent and biologically plausible, but interventional evidence
remains insufficient to establish causal efficacy. Future RCTs specifically designed to
evaluate MedDiet effects on testosterone in obese men—with adequate statistical power,
standardised dietary assessment, and hormonal endpoints—are urgently needed.

4.1. Potential Clinical Recommendations

• Consider VLCKD (8–16 weeks) as an initial dietary strategy for obese men with MOSH
and BMI ≥ 35 kg/m2 or concomitant metabolic syndrome, where available evidence
suggests greater consistency in testosterone restoration. This recommendation should
be applied on an individualised basis under medical supervision, with particular
caution in patients with diabetes or cardiovascular comorbidities.
• IF protocols (16:8 TRE or 5:2) may be considered for obese men with MOSH who
cannot adhere to VLCKD or who prefer a less restrictive dietary approach, given
evidence of comparable metabolic benefits and greater dietary flexibility. It should be
noted, however, that direct comparative data for testosterone outcomes between IF
and VLCKD remain limited and currently prevent definitive superiority claims for
either approach.
• Transition to a MedDiet-based dietary pattern following the active weight loss phase
(VLCKD or IF) may be considered to support maintenance of metabolic and hormonal
gains, given its superior long-term adherence profile and well-established cardiovas-
cular protective effects. This proposed sequential dietary strategy requires prospective
validation in adequately powered trials with hormonal primary endpoints before it
can be considered a formal evidence-based recommendation.

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• Monitoring: Serum total testosterone, calculated or directly measured free testosterone,

SHBG, LH, FSH, and metabolic parameters (fasting glucose, fasting insulin, lipid pro-
file, body weight, BMI) should be assessed at baseline and at 8–12 weeks after dietary
intervention initiation to evaluate hormonal response and guide further manage-
ment. Calculated free testosterone using the Vermeulen equation is recommended as a
complement to total testosterone measurement, given the known SHBG suppression
associated with obesity and its expected rise with metabolic improvement.

4.2. Limitations
This systematic review has several limitations that should be considered when inter-
preting its findings. First, the heterogeneity of dietary interventions, study populations,
and outcome reporting precluded formal meta-analysis for most comparisons. Second,
the quality of evidence for MedDiet testosterone effects is predominantly observational,
limiting causal inference. Third, no head-to-head RCTs directly comparing all three dietary
patterns with testosterone as the primary outcome were identified, representing a critical
evidence gap. Fourth, most studies had follow-up durations of 12–24 weeks, insufficient to
assess long-term hormonal sustainability. Fifth, publication bias may have inflated positive
findings, particularly for VLCKD studies. Sixth, this review was not prospectively regis-
tered in PROSPERO, which represents a significant methodological limitation regarding
transparency and replicability of the review protocol. Seventh, searches were restricted
to SciSpace, Google Scholar, and PubMed; the absence of EMBASE, Web of Science, the
Cochrane Library, and Scopus may have resulted in incomplete retrieval of the available ev-
idence base. Eighth, the majority of included studies reported only total serum testosterone
without measurement of free testosterone or SHBG, potentially underestimating the true
hormonal benefit of dietary intervention in a population characterised by obesity-related
SHBG suppression. Ninth, adherence to dietary interventions was inconsistently monitored
across studies, limiting the ability to establish dose–response relationships between dietary
compliance and hormonal outcomes. Tenth, the included study populations were predomi-
nantly of European and North American origin, which may limit the generalisability of
findings to other ethnic groups, given known population-level differences in testosterone
reference ranges and metabolic responses to dietary intervention.

4.3. Future Research Directions

• Head-to-head RCTs directly comparing MedDiet, VLCKD, and IF with total testos-
terone as the primary outcome in obese men with confirmed MOSH.
• Long-term follow-up studies (≥12 months) to assess the durability of testosterone
improvements and the impact of dietary transitions.
• Mechanistic studies investigating the direct effects of ketone bodies on HPG axis
function, independent of weight loss.
• Personalised medicine approaches identifying genetic, metabolomic, or microbiome
predictors of testosterone response to specific dietary interventions.
• Combination strategies evaluating the sequential use of VLCKD (induction) followed
by MedDiet (maintenance) on long-term testosterone and metabolic outcomes.

5. Conclusions
This systematic review suggests that dietary intervention may represent a clinically
relevant, evidence-informed, and potentially reversible approach to the management of
MOSH. Among the three dietary patterns evaluated, VLCKD provides the most consis-
tent available evidence for testosterone restoration in obese men, primarily through rapid
weight loss, improved insulin sensitivity, reduced systemic inflammation, and potential

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direct effects of nutritional ketosis on the HPG axis. Overall certainty of evidence is moder-
ate, reflecting heterogeneity across included studies, and clinical recommendations must
therefore be applied with appropriate individualisation and caution. Intermittent fasting
represents a clinically viable alternative with meaningful hormonal and metabolic benefits,
particularly for patients who cannot adhere to VLCKD. The Mediterranean diet, while
offering the most favourable long-term safety and adherence profile, currently lacks robust
interventional evidence for direct testosterone improvement in obese men and may be
best positioned as a maintenance strategy following active weight loss. Importantly, the
evidence base reviewed herein is predominantly biochemical in nature; reported outcomes
are centred on changes in serum testosterone concentration, with only limited and incon-
sistent data available on patient-relevant clinical endpoints—including sexual function,
resolution of hypogonadal symptoms, body composition changes, fertility parameters,
and health-related quality of life. The clinical significance of the biochemical testosterone
improvements documented in this review therefore remains to be established in adequately
powered trials employing validated clinical outcome measures as co-primary endpoints
alongside hormonal biochemistry.
The overarching clinical message is that weight loss—irrespective of the dietary strat-
egy employed—is the primary driver of testosterone recovery in MOSH, and clinicians
should prioritise the dietary approach most likely to achieve and sustain meaningful
weight reduction in each individual patient. It should be recognised, however, that the
degree of hormonal response is highly variable between individuals, and testosterone
normalisation cannot be guaranteed even with substantial weight loss; men with persis-
tent hypogonadism despite adequate weight reduction should undergo comprehensive
re-evaluation to exclude organic causes and to consider alternative therapeutic strategies.
Future head-to-head RCTs with hormonal primary endpoints are essential to definitively
establish the optimal dietary strategy for MOSH management; such trials should include
both free testosterone and total testosterone as co-primary endpoints, utilise standardised
measurement methodologies, and incorporate follow-up durations of at least 52 weeks to
assess long-term hormonal sustainability.

Supplementary Materials: The following supporting information can be downloaded at: https:
//[Link]/article/10.3390/nu18152417/s1. Supplementary Material S1 (Table S1): Complete
database search strings for SciSpace, Google Scholar, and PubMed. Supplementary Material S2
(Table S2): Standardised data extraction form and extracted data tables for all 52 included studies.
Supplementary Material S3 (Table S3): Risk of bias assessment for included RCTs using the Cochrane
RoB 2 tool. Supplementary Material S4 (Table S4): Newcastle–Ottawa Scale scores for included
observational studies. Supplementary Material S5 (Table S5): AMSTAR-2 appraisal results for
included systematic reviews and meta-analyses. Supplementary Material S6 (Table S6): Completed
PRISMA 2020 checklist with section and page references.

Author Contributions: Conceptualisation, S.L.V. and R.A.C.; methodology, S.L.V. and R.A.C.; investi-
gation, S.L.V. and R.A.C.; data curation, S.L.V. and R.A.C.; writing—original draft preparation, S.L.V.;
writing—review and editing, R.A.C.; supervision, S.L.V. All authors have read and agreed to the
published version of the manuscript.

Funding: This research received no external funding.

Institutional Review Board Statement: Not applicable.

Informed Consent Statement: Not applicable.

Data Availability Statement: No new data were created or analyzed in this study. Data sharing is
not applicable.

Conflicts of Interest: The authors declare no conflicts of interest.

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Nutrients 2026, 18, 2417 12 of 14

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