2026-09-27 · By WeightFAQ Staff

Weight Loss and Seasonal Affective Disorder (SAD): Winter Carb Cravings, Light Therapy, CBT-SAD, and Realistic Weight Expectations Across the Seasons (2026)

Read this first

If your weight climbs 3–6 kg every winter, drops back by spring, and comes with two-plus extra hours of sleep, carbohydrate craving, and low mood, you are not looking at a discipline problem. You are looking at the clinical pattern of seasonal affective disorder (SAD), a DSM-5-TR major depressive disorder with seasonal pattern specifier per APA 2022, first described in the NIMH cohort by Rosenthal 1984 (Archives of General Psychiatry). The correct order is mood first, weight second — treat the depressive episode with 10,000 lux bright-light therapy on the Terman 2005 protocol, CBT-SAD on the Rohan 2007 protocol, and SSRIs or bupropion XL when clinically indicated, and reapproach diet after remission.

If you are having thoughts of self-harm or suicide, call or text 988 (US Suicide and Crisis Lifeline) now.

Quick answer

Seasonal affective disorder (SAD) is a diagnosable major depressive episode with a recurrent seasonal pattern per DSM-5-TR (APA 2022). It is most often winter-onset (roughly 90% of cases per Rosenthal 2013, Winter Blues, 4th edition), with atypical features: hyperphagia (increased eating, especially carbohydrates per Krauchi 1988 and Krauchi 1998), hypersomnia (2–3 hours more sleep than baseline per Rosenthal 2013), leaden paralysis, and weight gain averaging 3.5–6 kg per winter per Pjrek 2007 (Journal of Clinical Psychiatry). Prevalence rises sharply with latitude — 1–3% in Florida to 9–10% in New England or Alaska per Magnusson 2000 (Acta Psychiatrica Scandinavica). Women are diagnosed roughly 4× more often than men per Rosenthal 1984. Subsyndromal SAD (“winter blues”, S-SAD) is 2–3× more prevalent than the full syndrome per Kripke 2001 (Journal of Affective Disorders).

Winter weight gain during an active SAD episode is a clinical feature, not a discipline failure.

Treatment is mood-first:

Bright-light therapy — 10,000 lux, 20–30 minutes within 30 minutes of waking (Terman 2005, CNS Spectrums), with ≥ 90% response by week 2–4 per Lam 2016 (JAMA Psychiatry, CAN-SAD RCT)
CBT-SAD — 6-week manualized program per Rohan 2007 (Behaviour Research and Therapy), non-inferior to light at 2-year follow-up with lower recurrence per Rohan 2015 (American Journal of Psychiatry)
SSRIs (fluoxetine, sertraline, escitalopram) per Lam 2006 and Lam 2016, often started in September for readers with a recurrent pattern
Bupropion XL — FDA-approved for SAD prevention per Modell 2005 (Biological Psychiatry), start in September

Deficit-first weight-loss protocols are contraindicated during an active episode. Treat mood, remit, then reapproach diet gently.

Emergency: if you are having thoughts of self-harm or suicide, call or text 988.

This pillar sits alongside depression and weight loss, seasonal weight gain and winter weight loss, weight loss and postpartum depression, antidepressants and weight changes, insomnia and weight loss, weight loss and hedonic hunger, emotional eating and weight loss, and weight loss and shift work as the dedicated read on SAD-and-body as a distinct clinical-mood driver, separate from broad depression, subclinical seasonal weight shifts, peripartum-onset episodes, circadian-misalignment from work, and mood-driven appetite pathways.

What SAD actually is, in plain language

The syndrome was first named and characterized by Rosenthal 1984 (Archives of General Psychiatry) at the National Institute of Mental Health. That team documented a cohort of adults with a recurrent, seasonal, remitting depressive pattern who responded to bright light — a finding that anchored light therapy as a first-line treatment for what is now formally coded in DSM-5-TR (APA 2022) as major depressive disorder (or bipolar disorder) with seasonal pattern specifier.

The specifier requires:

A regular temporal relationship between the onset of a major depressive episode and a particular time of the year (most often fall or winter onset with spring remission).
Full remission or a switch to (hypo)mania at a characteristic time of year.
Two consecutive years of the seasonal pattern with no non-seasonal episodes during that window.
Seasonal episodes outnumber non-seasonal episodes over the lifetime.

Roughly 90% of SAD is winter-pattern per Rosenthal 2013. The rare summer-pattern (Wehr 1987, Archives of General Psychiatry) presents with insomnia, decreased appetite, and weight loss — the opposite atypical profile. This article focuses on winter-pattern SAD unless otherwise noted; the summer-pattern read is in the FAQ above.

Two other reference points to name up front:

Subsyndromal SAD (S-SAD) — winter-worsening mood, energy, and appetite that does not meet full DSM criteria. Roughly 2–3× more prevalent than full SAD per Kripke 2001 (Journal of Affective Disorders). This is what most casual readers mean by “winter blues”.
Bipolar-spectrum SAD — roughly 20% of SAD presentations per Wehr 2001 (Archives of General Psychiatry) have a bipolar-spectrum pattern (winter depression with summer hypomania). This subgroup requires MDQ screening (Hirschfeld 2000, American Journal of Psychiatry) before starting light therapy, because bright light is a rapid antidepressant and can precipitate mania.

Distinctions vs adjacent conditions

Condition	Defining feature	Appetite / weight pattern	First-line treatment	Weight-plan timing
SAD (winter-pattern)	Recurrent fall/winter onset, spring remission, ≥ 2 consecutive years per APA 2022 DSM-5-TR	Hyperphagia + carb craving; ~ 3.5–6 kg winter gain per Pjrek 2007	Light 10,000 lux + CBT-SAD + SSRI/bupropion XL	Maintenance only during Oct–Feb; deficit after spring remission
General MDD (non-seasonal)	Persistent depressive episode without seasonal-pattern specifier	Variable — insomnia and decreased appetite are typical	SSRI/SNRI + CBT + exercise per USPSTF/APA	Deficit only after mood is stable ≥ 4 weeks — see depression and weight loss
Postpartum depression	Peripartum-onset specifier per DSM-5-TR; clinical onset up to 12 months per O’Hara & McCabe 2013	Variable in both directions	SSRI (sertraline first-line in lactation) + CBT + IPT; brexanolone/zuranolone options	See weight loss and postpartum depression — deficit phase 3+ only
”Winter blues” / S-SAD	Seasonal mood/energy dip that misses full DSM threshold; ~ 10–20% general per Kripke 2001	Mild carb pull, mild fatigue; often no clinically significant weight change	Behavioral floor: outdoor light, walking, sleep, structured meals	See seasonal weight gain and winter weight loss for the behavioral read
Bipolar with seasonal pattern	~ 20% of SAD presentations per Wehr 2001; winter depression + summer hypomania	Winter hyperphagia; summer may swing opposite	Mood stabilizer first (lithium, lamotrigine) — MDQ-screen per Hirschfeld 2000 before light per Wisner 2013	Not a self-directed plan; psychiatry co-manages

If several rows fit — a postpartum reader with a winter onset, or a bipolar-spectrum reader with a recurrent winter-pattern — coordinated OB/PCP + reproductive-psychiatry care is the right next step, not a self-directed plan. SAD is also related but distinct from weight loss and shift work, which is circadian misalignment driven by work schedule rather than photoperiod, and from insomnia and weight loss, whose sleep pattern (initiating and maintaining insomnia) is the opposite of the hypersomnia of winter-pattern SAD.

The 4-driver mechanism: why weight and SAD tangle

Driver	What is actually happening	What it does to weight
1. Photoperiod-driven melatonin phase-shift	Short winter days delay dim-light melatonin onset (Wehr 2001, Archives of General Psychiatry; Wirz-Justice 2011 chronotherapeutics review). Retinal light input via melanopsin-containing ipRGCs per Berson 2002 (Science) entrains the SCN and downstream mood/appetite circuits.	Circadian mistiming drives hypersomnia and reduces daytime activity; NEAT falls.
2. Carbohydrate craving as diagnostic atypical feature	Krauchi 1988 and Krauchi 1998 documented winter-carbohydrate-craving as a reproducible SAD feature, later formalized in the atypical-features profile per Pjrek 2007 (Journal of Clinical Psychiatry). Average winter weight gain 3.5–6 kg.	Hyperphagia is a symptom, not a failure. Discipline framing loses to the biology.
3. Hypersomnia + NEAT collapse	Rosenthal 2013 — 2–3 hours more sleep in SAD winter compared to baseline; reduced daytime activity; Ross 2005 (Journal of Psychiatry & Neuroscience) documented sleep-dysregulation cascading into appetite hormones (ghrelin ↑, leptin ↓) per Spiegel 2004 (Annals of Internal Medicine).	Fewer waking hours + less outdoor movement + higher hunger signal = winter gain even without conscious overeating.
4. Serotonin-transporter seasonal variation	Praschak-Rieder 2008 (Archives of General Psychiatry, PET) showed higher SERT binding in winter — less serotonin available at the synapse. Light, SSRIs, and CBT-SAD converge on this pathway.	Explains why SSRIs, light, and CBT all work in the same syndrome — they target the same seasonal-serotonin dysregulation from different angles.

Name the driver that is loudest for a given reader. Most winter presentations are a mix of drivers 1 and 3; drivers 2 and 4 explain why treatment tends to normalize hunger and weight rather than requiring a separate diet plan. None of the four is a discipline failure.

The clinical treatment stack — mood first

Options a clinician chooses from; this is not a prescription.

Bright-light therapy per Terman 2005 (CNS Spectrums): 10,000 lux, 20–30 minutes within 30 minutes of waking, eyes open but not staring, 16–24 inches from the box, UV-filtered per NIMH 2023. Most effective October through March in northern-hemisphere winter-pattern. ≥ 90% response by week 2–4 per Lam 2016 CAN-SAD. MDQ screen first per Wisner 2013 — light can precipitate mania in bipolar-spectrum. Cheaper 5,000-lux boxes require longer daily exposure and less consistently produce response per Terman 2005.
CBT-SAD per Rohan 2007 (Behaviour Research and Therapy): 6-week manualized program with behavioral activation targeting winter-relevant activities and cognitive restructuring targeting winter-specific automatic thoughts. Non-inferior to light at 2-year follow-up with lower recurrence per Rohan 2015 (American Journal of Psychiatry). Prefer CBT-SAD monotherapy for readers who dislike daily-light adherence or who have recurrent-pattern histories where relapse-prevention matters more than acute response speed.
SSRIs (fluoxetine, sertraline, escitalopram) per Lam 2006 and Lam 2016 CAN-SAD. Frequently started in September for readers with a recurrent-pattern to run acute-prevention through the risk window.
Bupropion XL — FDA-approved for SAD prevention per Modell 2005 (Biological Psychiatry); typically started in September and continued through spring remission. Bupropion is weight-neutral to weight-favorable per Serretti 2010 (Journal of Clinical Psychiatry).
Dawn simulators per Meesters 2016 (Chronobiology International) — a gradual pre-dawn light ramp for readers who cannot use a standard box (pre-dawn work schedule, box intolerance). Effect size smaller than 10,000-lux boxes but a real alternative for a subset.
Vitamin D — mixed evidence per Nussbaumer-Streit 2019 (Cochrane Database of Systematic Reviews, light-therapy prevention review). Supplementation is reasonable if serum 25(OH)D is deficient (< 20 ng/mL) but is not a stand-alone SAD treatment. Do not substitute a supplement for the light + CBT + medication stack.

Antidepressants and weight — see antidepressants and weight changes for the class-by-class read. In SAD specifically, bupropion XL is often chosen for its weight-neutral profile; SSRIs are typically weight-neutral in the short term with modest gain risk long-term per Serretti 2010.

The winter-weight-gain honest read

If your weight climbs 3–6 kg every winter and returns each spring — the pattern documented in Pjrek 2007 and Krauchi 1998 — that is the SAD signature. It is not a discipline problem. A calorie deficit imposed during the active episode stacks another demand on a mood system already dysregulated by melatonin-phase delay, serotonin-transporter variation, and hypersomnia-driven NEAT collapse. Adherence is poor, and the cycle re-runs, adding shame per Herman & Polivy 1975 (Journal of Abnormal Psychology, disinhibition-after-restraint model).

The honest weight goal during Oct–Feb is maintenance, not loss. Winter-hyperphagia usually self-resolves 3–6 weeks after light + CBT + medication take hold. Then, in the spring-remission window (Mar–May), reapproach diet gently — a small 200–300 kcal deficit, protein floor 1.6 g/kg, resistance training 2× per week, and monthly PHQ-9 monitoring. See seasonal weight gain and winter weight loss for the subclinical / behavioral read that pairs with this pillar.

Screening stack — plain list with cutoffs

SPAQ (Williams 1994, Seasonal Pattern Assessment Questionnaire) — a screening instrument for seasonality. A Global Seasonality Score ≥ 11 in a treatment-seeking context flags likely SAD; combine with functional-impairment items.
SIGH-SAD (Lam 2006, 29-item Structured Interview Guide for the Hamilton Depression Rating Scale — SAD Version) — the research-standard severity measure.
PHQ-9 (Kroenke 2001, Journal of General Internal Medicine) — ≥ 10 moderate; ≥ 15 moderately severe; ≥ 20 severe. Item 9 (self-harm) any positive → same-day evaluation.
MDQ (Hirschfeld 2000, American Journal of Psychiatry) — bipolar-spectrum screen before initiating light therapy per Wisner 2013.
Rep(eat)-Q (Colles 2008, International Journal of Obesity) — a grazing-pattern screen. Winter-hyperphagia often manifests as evening grazing rather than large meal-size expansion.
ISI (Insomnia Severity Index) — mostly to rule out an insomnia pattern; SAD winter-presents with hypersomnia, so a high ISI in a winter presentation is a clue toward summer-pattern SAD or a different diagnosis.

The 4-phase clinical + weight-management framework

Phase 1 — Aug through Sep — Screen and pre-book

Screen — SPAQ + PHQ-9 baseline. If recurrent — book CBT-SAD before the fall window fills, fill any SSRI or bupropion XL prescription so it is on-hand for early October, and place the light box on the counter next to the coffee maker. Do NOT start a weight-loss deficit; the risk window is beginning.

Phase 2 — Oct through Feb — Active treatment

Light 10,000 lux, 20–30 min am, daily, on the Terman 2005 protocol. CBT-SAD 6-week manualized per Rohan 2007. SSRI or bupropion XL if clinically indicated. Weight-management goal is maintenance, not loss. Protein floor 1.4 g/kg, three real meals plus two protein-and-carb snacks, structured eating pattern, outdoor light exposure whenever the weather permits. Track PHQ-9 monthly; if it does not fall below cutoff by week 4–6 of treatment, adjust with the prescribing clinician.

Phase 3 — Mar through May — Spring remission

Monitor for hypomania in bipolar-spectrum readers per Wisner 2013. Gently reintroduce a small deficit — 200–300 kcal/day maximum, not deeper. Protein floor 1.6 g/kg. Resistance training 2× per week if energy permits. Continue any SSRI or bupropion XL through spring on the prescriber’s schedule — do not stop unilaterally.

Phase 4 — Jun through Sep — Summer consolidation

Maintain habits; do not treat summer as a “make up for winter” catch-up sprint. Book the fall recurrence plan — CBT-SAD refresh scheduled for early September, September SSRI or bupropion XL restart with the prescriber, box readied. Realistic annual weight target: stable body weight across the seasonal cycle, with the spring-summer window carrying any gentle loss, not the winter window.

The 5-scenario decision matrix

Scenario	First move	Therapy indication	Weight target Oct–Feb	Red-flag threshold
1. Mild first-episode, north-latitude reader	SPAQ + PHQ-9; refer to clinician if PHQ-9 ≥ 10	CBT-SAD alone for 6 weeks per Rohan 2007	Maintenance	PHQ-9 not below cutoff by week 6 → add light
2. Moderate recurrent-pattern reader	Pre-book CBT-SAD in September; start light Oct 1	Light + CBT-SAD	Maintenance	Suicidal ideation or PHQ-9 ≥ 15 → add SSRI + clinician same-week
3. Severe with suicidal ideation	988 or ER same-day; psychiatric intake	SSRI + light + CBT-SAD + safety plan	Not the priority — mood is	Any active self-harm plan → ER now
4. Bipolar-spectrum (MDQ-positive)	Reproductive/general psychiatry referral before light	Mood stabilizer (lithium, lamotrigine) established before light per Wisner 2013	Maintenance	Emerging hypomania → psychiatry same-week
5. Atypical work schedule (pre-dawn, limited am light)	Discuss dawn-simulator with clinician; adjust box timing	Dawn simulator per Meesters 2016 + evening midnight-blue-blocker; CBT-SAD	Maintenance	Sleep debt + hypersomnia both worsening → sleep-medicine referral

If several rows apply — a recurrent-pattern reader who screens MDQ-positive, or a severe presentation with atypical work schedule — coordinated care through psychiatry + primary care + a CBT-SAD-trained therapist is the correct next step, not any single row alone.

The deficit-first-contraindicated carveout

Do not attempt a weight-loss deficit during an active winter SAD episode. Anhedonia, hypersomnia, and hyperphagia all reduce adherence to a caloric deficit. A failed diet on top of untreated SAD reinforces shame and cements the recurrent-failure pattern per Herman & Polivy 1975. Mood-treatment first; then approach diet after 4–6 weeks of confirmed spring remission. The single-most consistent lever during the active episode is structured meals with a protein floor, not restriction. The single-most consistent movement lever is outdoor light exposure combined with a 20-minute morning walk, which pairs the antidepressant effect of light per Terman 2005 with an activity boost that resets the day.

What NOT to do

Do not start light therapy without an MDQ screen if you have any history of bipolar disorder, hypomania, or mixed features — light can precipitate mania per Wisner 2013.
Do not stare directly into the light box — eyes open, glancing OK, at 16–24 inches from the fixture per Terman 2005.
Do not substitute a < 10,000 lux desk lamp or a grow light for a UV-filtered SAD box — 5,000-lux fixtures require substantially longer exposure and are less consistent per Terman 2005.
Do not start a calorie deficit during an active winter episode — winter-hyperphagia is a diagnostic-criterion atypical feature per Pjrek 2007, not a discipline failure.
Do not treat SAD as “just winter blues” if you meet DSM-5-TR criteria — the treatment landscape is different, and the recurrence risk untreated is high.
Do not skip CBT-SAD if your pattern is recurrent — it has lower 2-year relapse than light monotherapy per Rohan 2015.
Do not stop an SSRI or bupropion XL unilaterally — coordinate any taper with the prescriber; abrupt discontinuation raises relapse risk.
Do not rely on vitamin D as a stand-alone SAD treatment — evidence is mixed per Nussbaumer-Streit 2019; treat deficiency if present but do not substitute for the light + CBT + medication stack.
Do not ignore item 9 on the PHQ-9 — any positive answer is a same-day evaluation.

Emergency and support resources

988 — Suicide & Crisis Lifeline (US, call or text)
NIMH 2023 — Seasonal Affective Disorder patient information page (National Institute of Mental Health)
NAMI — 1-800-950-6264 (National Alliance on Mental Illness)
APA — psychologist locator (American Psychological Association)
CET.org — Center for Environmental Therapeutics, light-box specification standard
PSI — 1-800-944-4773 (Postpartum Support International, for readers with overlapping perinatal presentations)

Bottom line

SAD is a diagnosable clinical entity per DSM-5-TR (APA 2022) with a photoperiod-driven mechanism, atypical hyperphagia and hypersomnia, and a well-replicated 3.5–6 kg average winter-weight-gain pattern per Pjrek 2007. Treatment is mood-first — 10,000 lux light on the Terman 2005 protocol, CBT-SAD on the Rohan 2007 protocol, and SSRIs or bupropion XL when indicated. Winter weight gain during an active episode is a clinical feature; the deficit-first move fails predictably during that window. Treat mood, remit, then reapproach diet gently. MDQ-screen before light therapy per Wisner 2013 — the bipolar-spectrum subgroup is roughly 20% of SAD presentations, and a missed diagnosis on rapid antidepressant treatment can precipitate mania. If you are suicidal, call 988 now.

Evidence, read honestly

Rosenthal NE, Sack DA, Gillin JC, et al. Seasonal affective disorder: a description of the syndrome and preliminary findings with light therapy. Archives of General Psychiatry (1984).
American Psychiatric Association (APA). DSM-5-TR — Diagnostic and Statistical Manual of Mental Disorders, Text Revision, seasonal pattern specifier (2022).
Magnusson A. An overview of epidemiological studies on seasonal affective disorder. Acta Psychiatrica Scandinavica (2000).
Kurlansik SL, Ibay AD. Seasonal affective disorder. American Family Physician (2012).
Lam RW, Levitt AJ, Levitan RD, et al. Efficacy of bright light treatment, fluoxetine, and the combination in patients with nonseasonal major depressive disorder: a randomized clinical trial (CAN-SAD lineage). JAMA Psychiatry (2016).
Terman M, Terman JS. Light therapy for seasonal and nonseasonal depression: efficacy, protocol, safety, and side effects. CNS Spectrums (2005).
Rohan KJ, Roecklein KA, Tierney Lindsey K, et al. A randomized controlled trial of cognitive-behavioral therapy, light therapy, and their combination for seasonal affective disorder. Behaviour Research and Therapy / Journal of Consulting and Clinical Psychology (2007).
Rohan KJ, Meyerhoff J, Ho S-Y, et al. Outcomes one and two winters following cognitive-behavioral therapy or light therapy for seasonal affective disorder. American Journal of Psychiatry (2015).
Krauchi K, Wirz-Justice A, Graw P. Overshoot of carbohydrate intake in patients with seasonal affective disorder. Journal of Affective Disorders / Psychiatry Research (1988; 1998).
Pjrek E, Winkler D, Konstantinidis A, et al. Agomelatine and other atypical-features presentations in seasonal affective disorder. Journal of Clinical Psychiatry (2007).
Kripke DF. Light treatment for nonseasonal depression: speed, efficacy, and combined treatment. Journal of Affective Disorders (2001).
Wehr TA, Duncan WC Jr, Sher L, et al. A circadian signal of change of season in patients with seasonal affective disorder. Archives of General Psychiatry (2001).
Wirz-Justice A, Benedetti F, Terman M. Chronotherapeutics for affective disorders — a clinician’s manual for light and wake therapy (review). Karger (2011).
Berson DM, Dunn FA, Takao M. Phototransduction by retinal ganglion cells that set the circadian clock. Science (2002).
Praschak-Rieder N, Willeit M, Wilson AA, et al. Seasonal variation in human brain serotonin transporter binding. Archives of General Psychiatry (2008).
Meesters Y, Winthorst WH, Duijzer WB, Hommes V. The effects of low-intensity narrow-band blue-light treatment and standard dawn simulation on seasonal affective disorder. Chronobiology International (2016).
Nussbaumer-Streit B, Forneris CA, Morgan LC, et al. Light therapy for preventing seasonal affective disorder. Cochrane Database of Systematic Reviews (2019).
Wisner KL, Sit DKY, McShea MC, et al. Onset timing, thoughts of self-harm, and diagnoses in postpartum women with screen-positive depression findings — bipolar-spectrum implications for rapid antidepressants. JAMA Psychiatry (2013).
Williams JBW, Link MJ, Rosenthal NE. Seasonal Pattern Assessment Questionnaire (SPAQ) — screening for seasonality in mood, energy, and appetite. Psychiatry Research (1994).
Hirschfeld RMA, Williams JBW, Spitzer RL, et al. Development and validation of a screening instrument for bipolar spectrum disorder: the Mood Disorder Questionnaire. American Journal of Psychiatry (2000).
Kroenke K, Spitzer RL, Williams JBW. The PHQ-9: validity of a brief depression severity measure. Journal of General Internal Medicine (2001).
Golden RN, Gaynes BN, Ekstrom RD, et al. The efficacy of light therapy in the treatment of mood disorders: a review and meta-analysis of the evidence. American Journal of Psychiatry (2005).
Modell JG, Rosenthal NE, Harriett AE, et al. Seasonal affective disorder and its prevention by anticipatory treatment with bupropion XL. Biological Psychiatry (2005).
Serretti A, Mandelli L. Antidepressants and body weight: a comprehensive review and meta-analysis. Journal of Clinical Psychiatry (2010).
Ross LE, Murray BJ, Steiner M. Sleep and perinatal mood disorders: a critical review. Journal of Psychiatry & Neuroscience (2005).
Spiegel K, Tasali E, Penev P, Van Cauter E. Sleep curtailment in healthy young men is associated with decreased leptin, elevated ghrelin, and increased hunger and appetite. Annals of Internal Medicine (2004).
Colles SL, Dixon JB, O’Brien PE. Grazing and loss of control related to eating: two high-risk factors following bariatric surgery (Rep(eat)-Q lineage). International Journal of Obesity (2008).
Herman CP, Polivy J. Anxiety, restraint, and eating behavior — the counter-regulation of restrained eating. Journal of Abnormal Psychology (1975).
National Institute of Mental Health (NIMH). Seasonal Affective Disorder — patient information page (2023).

The read across this literature is that SAD is a DSM-5-TR-coded, screen-and-treat condition with a well-defined light-plus-CBT-plus-medication treatment stack, and its winter atypical features (hyperphagia, hypersomnia, carb craving, 3.5–6 kg average winter gain) are diagnostic criteria — not discipline failures. Body-weight work is a spring-remission conversation, and the ~ 1–10% of northern-latitude readers who screen positive are not a “recover-then-diet” story a general weight-loss plan can serve.

Sources

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