The 9 pm kitchen visit after a bad day is not a failure of discipline. It is a hormone doing what it evolved to do. Cortisol rises under stress, cortisol makes energy dense food more appealing, and eating that food turns the stress response down. The loop closes, the relief is real, and by the next evening it is ready to run again.
GLP-1 receptor agonists arrive in the middle of this loop from an unexpected direction. GLP-1 receptors are dense in the hypothalamic paraventricular nucleus and the brainstem, the two regions that launch the cortisol response, and dense in the reward circuitry that makes comfort food comforting. A drug that acts on both can, in principle, change how stress feels, how the body responds to it, and what a person does about it. The animal literature shows an acute stimulation of the stress axis that habituates with repeated dosing. The human trial literature shows reduced cravings, improved control of eating, and no signal of harm to mood.
This article sets out what cortisol does across a normal day, how stress eating works, what is known about GLP-1 agonists and the hypothalamic pituitary adrenal axis in humans and animals, why the dose ramp and the size of the calorie deficit both matter to the stress axis, and where sleep and exercise intensity fit. The figures come from the prescribing information, the STEP and SURMOUNT programmes, and the stress physiology literature, and the article is explicit about which charts are measurements and which are models.
Key Takeaways
- Stress eating is a physiological loop, not a character flaw. Cortisol increases the appeal of high fat, high sugar food, and eating that food dampens the hypothalamic pituitary adrenal response, which is why Dallman and colleagues described comfort food as self medication. In the 2013 American Psychological Association survey, 38 percent of US adults reported overeating or eating unhealthy food because of stress in the previous month.
- GLP-1 receptor agonists act on both ends of the loop. Central GLP-1 signalling acutely activates the stress axis in rodents and an exendin-4 infusion raised ACTH and cortisol in healthy volunteers in the Gil-Lozano 2010 study, but the effect is dose dependent, habituates with repeated exposure, and has produced no sustained cortisol signal in the long GLP-1 trials.
- The drugs reduce the pull of the food rather than the stress. In the two year STEP 5 analysis, semaglutide 2.4 mg improved craving control and reduced cravings for savoury food compared with placebo on the Control of Eating Questionnaire, consistent with an effect on reward circuitry rather than on the stressor.
- Mood safety is well established at the population scale. Psychiatric adverse events matched placebo across the STEP and SURMOUNT programmes, the FDA's 2024 review found no causal link to suicidal thoughts, and Wang and colleagues reported a 73 percent lower rate of first-time suicidal ideation in semaglutide users than in users of other weight loss drugs.
- The calorie deficit is itself a stressor. Tomiyama and colleagues found that restricting to 1,200 kcal a day for three weeks raised cortisol output, while tracking calories raised perceived stress. A low dose that produces a moderate, appetite led deficit is a gentler input to the stress axis than an aggressive cut.
- Sleep is the strongest cortisol lever available. One night of four hours in bed raised next evening cortisol by 37 percent and total sleep loss raised it by 45 percent in Leproult et al 1997, and evening cortisol is the part of the rhythm most closely tied to late eating and visceral fat.
What is cortisol doing across a normal day?
A morning surge, a long decline, and a floor that stress raises
Cortisol follows a steep daily rhythm: it peaks within the first hour after waking, falls through the afternoon, and reaches its lowest point around midnight. Serum cortisol in a healthy adult sits near 10 to 20 micrograms per decilitre in the morning and below 5 late in the evening. The rhythm is driven by the suprachiasmatic nucleus, the brain's master clock, acting through the hypothalamus and pituitary, and it is the shape of the curve rather than any single value that reflects how the stress axis is functioning.
The most studied feature of the curve is the cortisol awakening response. Salivary cortisol rises by roughly 50 to 75 percent in the 30 to 45 minutes after waking, according to the review by Clow and colleagues, then falls back. The awakening response prepares the body for the demands of the day, mobilising glucose and sharpening attention, and it is one reason the first hour after waking is when hunger is naturally lowest for many people. A blunted awakening response and a high evening floor together describe the flattened rhythm found in chronic stress, burnout, and short sleep.
The flattening matters for body composition because the evening is when cortisol's effects on appetite and fat storage are least opposed. Cortisol raises circulating glucose and free fatty acids, and in the presence of insulin it directs the resulting energy into fat, with a preference for the visceral depot. Visceral adipose tissue carries more glucocorticoid receptors than subcutaneous fat, a finding that goes back to Rebuffé-Scrive in 1985, and expresses more of the enzyme 11 beta HSD1, which regenerates active cortisol inside the fat cell. A rhythm that stays high into the night therefore favours abdominal fat, which is where the visceral fat article on this site picks up.
What Does a Healthy Cortisol Rhythm Look Like Next to a Flattened One?
Modelled serum cortisol in micrograms per decilitre across 24 hours. The healthy curve follows standard clinical reference ranges; the flattened curve follows the pattern described in chronic stress and short sleep studies
- Healthy rhythm
- Flattened rhythm (chronic stress, short sleep)
The flattened curve has a lower morning peak and a higher evening floor. Total daily cortisol may be similar between the two; what differs is the timing, and the evening excess is the part most associated with late eating and visceral fat. These are illustrative curves built from published reference ranges, not measurements from GLP-1 users.
How Big Is the Cortisol Awakening Response?
Modelled salivary cortisol in nmol/L across the first hour after waking, following the 50 to 75 percent rise that peaks 30 to 45 minutes after waking described in Clow et al 2004
The awakening response is a normal, healthy feature of the rhythm and one reason morning appetite is naturally low. It is blunted in burnout and chronic fatigue and exaggerated under acute anticipatory stress. Its size is unaffected by GLP-1 treatment in any published human study, because none has measured it.
How does stress drive eating?
Cortisol sets the appetite, food turns the cortisol down
Stress drives eating through a two way loop between cortisol and palatable food. Acute stress, the kind that lasts minutes, usually suppresses appetite through adrenaline and corticotropin releasing hormone. Chronic stress, the kind that lasts days to months, does the opposite. Sustained cortisol increases the motivation to eat and shifts preference toward foods high in fat and sugar, and eating those foods reduces activity in the hypothalamic pituitary adrenal axis. Dallman and colleagues laid this out in a 2003 review that gave comfort food its scientific definition: food eaten because it dampens the stress response.
The individual differences are large and they track cortisol. Epel and colleagues exposed 59 women to laboratory stress on three days and a control session on a fourth, then let them eat freely. Women whose cortisol rose most in response to stress ate more on the stress days than the low reactors, and chose more sweet food. In an earlier study the same group found that women with more abdominal fat, measured by waist to hip ratio, produced larger cortisol responses to the same stressor. High reactivity, stress eating, and central fat cluster together, which is the pattern many people recognise in themselves before they start a GLP-1.
The population numbers are not small. In the American Psychological Association's 2013 Stress in America survey, 38 percent of adults said they had overeaten or eaten unhealthy food because of stress in the previous month, and about half of those did so weekly or more. A third of the stress eaters said the food distracted them from the stress, and 27 percent of all adults described eating as a regular way of managing it. Stress eating is one of the most common eating behaviours in the country, and the food noise article on this site describes the intrusive, looping quality it takes on in the people most affected.
How Common Is Stress Eating?
Percent of US adults reporting each behaviour in the American Psychological Association Stress in America survey, 2013
The second and third bars are subsets of the first: of the 38 percent who stress ate, about half did so weekly and a third said the food served as a distraction. Skipping meals under stress, the last bar, is the acute stress pattern and often precedes an evening overeat once the cortisol response settles.
Does a GLP-1 change the stress response itself?
Acutely yes, chronically it habituates, and mood data are reassuring
A GLP-1 receptor agonist can acutely activate the stress axis, and the effect fades with repeated dosing. GLP-1 producing neurons in the brainstem project to the paraventricular nucleus of the hypothalamus, where corticotropin releasing hormone neurons launch the cortisol cascade, and those GLP-1 neurons fire in response to stressors. Ghosal, Myers, and Herman summarised the rodent evidence in 2013: central GLP-1 signalling is required for a full stress response, blocking it blunts corticosterone release, and giving a GLP-1 agonist raises corticosterone acutely in a dose dependent way. The same review noted that the response habituates with chronic administration, and that GLP-1 signalling in the amygdala contributes to anxiety like behaviour in the short term.
The human data are thinner but consistent. Gil-Lozano and colleagues infused exendin-4, the parent molecule of exenatide, into healthy volunteers and measured a rise in ACTH and cortisol over the following hours, matching what they saw in rats. That is an acute response to a rapid intravenous dose of a short acting agonist, and it is a long way from a small subcutaneous dose of a weekly drug that reaches its peak over one to three days. No published study has measured cortisol rhythms in people on semaglutide or tirzepatide, but the 68 to 72 week STEP and SURMOUNT trials found no clinical picture, no weight pattern, no blood pressure pattern, and no glucose pattern, that would suggest a sustained cortisol excess. The opposite pattern, with blood pressure, waist circumference, and glucose all falling, is what the trials report.
The concern that these drugs might worsen mood has been examined at scale and not supported. Psychiatric adverse events were similar between drug and placebo across the STEP programme, and the FDA's January 2024 review of its adverse event database concluded that the evidence did not show a causal link between GLP-1 drugs and suicidal thoughts. Wang, Volkow, and colleagues then analysed electronic health records for around 240,000 people with overweight or obesity and 1.6 million with type 2 diabetes. Semaglutide users had a 73 percent lower rate of first-time suicidal ideation than users of other weight loss drugs, and a 56 percent lower rate of recurrence. Those are associations in observational data, but they run firmly in the reassuring direction, and the mental health article on this site covers the neuroplasticity evidence behind them.
Is Semaglutide Associated With More or Less Suicidal Ideation Than Other Drugs?
Hazard ratios from Wang et al 2024, Nature Medicine, comparing semaglutide users with users of other weight loss drugs (obesity cohort) or other diabetes drugs (diabetes cohort). A value below 1.0 means fewer events in the semaglutide group
Every bar sits well below the line of no difference. The analysis used propensity matching to balance the groups on more than a hundred variables, but it remains observational: people prescribed semaglutide may differ from those prescribed other drugs in ways the matching could not capture. The randomised trials point the same way, with psychiatric events matching placebo.
Does a GLP-1 reduce stress eating specifically?
It weakens the pull of the food, not the stressor
A GLP-1 reduces stress eating by making the food less compelling, not by reducing the stress. The best evidence comes from the STEP 5 trial, in which Wharton and colleagues tracked the Control of Eating Questionnaire over two years. Semaglutide 2.4 mg improved craving control and reduced cravings for savoury food compared with placebo at week 104, with the largest gains in the first 20 weeks. Cravings for sweet food and positive mood improved early and then converged with placebo over the second year. The domain that held up, craving control, is the one that describes whether a person can resist a food once they want it, which is exactly the capacity that collapses under stress.
The mechanism runs through the reward system. GLP-1 receptors are expressed in the ventral tegmental area and nucleus accumbens, and in rodents GLP-1 agonists reduce dopamine release in response to palatable food and reduce the effort an animal will expend to obtain it. In human imaging studies, exenatide reduced the brain's response to pictures of high calorie food in the insula and putamen. The dopamine connection article on this site goes into that circuitry in detail. For stress eating, the relevant point is that cortisol's effect on food preference is delivered through the same reward pathway, so a drug that damps the pathway damps the cortisol driven urge along with every other urge.
This has a side that people rarely expect. When the comfort food stops working, the stress it was covering becomes more visible. Many people on a GLP-1 describe a flat or irritable stretch in the first months that is not depression and not a drug effect, but the experience of a stressor without its habitual buffer. Naming it helps. So does replacing the function the food served, because the cortisol loop does not care whether it is closed with a biscuit or a walk, and the walk lowers the evening floor while the biscuit raises it.
Why does the dose ramp matter for the stress axis?
A smaller acute stimulus, fewer restarts, and a gentler deficit
The dose ramp matters because the acute activation of the stress axis by GLP-1 agonists is dose dependent and habituates, so each escalation step delivers a fresh stimulus that the body then adapts to. The labelled Wegovy schedule steps semaglutide from 0.25 mg to 2.4 mg across five increases in 16 weeks, and the Zepbound schedule steps tirzepatide from 2.5 mg to as much as 15 mg. Each step brings a new peak in drug exposure, a new round of nausea for a proportion of people, and, on the animal data, a new acute nudge to corticosterone before habituation catches up. A protocol that holds at a fraction of the first labelled step meets that stimulus once, at a lower amplitude.
The second reason is nausea itself. Nausea is a stressor in the plain physiological sense: it activates the same brainstem GLP-1 neurons that drive the cortisol response, and a person who feels sick for two days after every escalation is spending those days with a raised stress axis. In the STEP 1 trial, 44 percent of the semaglutide group reported nausea against 16 percent on placebo, concentrated around the dose steps. The gentle ramp article on this site sets out how a slower, lower escalation reduces that burden.
The third reason is the deficit. Tomiyama and colleagues randomised women to three weeks of either restricting intake to 1,200 kcal a day or not, crossed with either tracking their calories or not. Restriction raised cortisol output regardless of tracking, and tracking raised perceived stress regardless of restriction. Dieting, in other words, is a stressor twice over. A GLP-1 removes the tracking, because the deficit comes from appetite rather than arithmetic, and a low dose produces a smaller deficit that sits closer to the range where the stress axis is unbothered. A 15 percent loss over 68 weeks at the full labelled dose is a large physiological event; a slower loss at a lower dose is a smaller one.
How Does the Labelled Escalation Compare With a Low Dose Protocol?
Weekly semaglutide dose in mg across the first 20 weeks under the labelled Wegovy schedule versus a representative low dose protocol. Each step in the labelled line is a fresh acute stimulus to the stomach and, on the animal data, to the stress axis
- Labelled Wegovy escalation
- Representative low dose protocol
The labelled line climbs almost tenfold in 16 weeks. The low dose line reaches a plateau at the first labelled step and stays there. The low dose figures are illustrative of protocols discussed on this site and have not been tested in trials; the labelled figures are from the Wegovy prescribing information.
How much does sleep move cortisol?
More than anything else that can be changed in a week
A single short night raises evening cortisol by more than a third. Leproult and colleagues kept healthy men in the laboratory for one night of normal sleep, one night with four hours in bed, and one night of total sleep loss, and measured plasma cortisol the following day. Partial sleep loss raised next evening cortisol by 37 percent and total sleep loss raised it by 45 percent, with the effect concentrated in the late afternoon and evening, and the rate at which cortisol fell after its morning peak was slowed sixfold. That is the flattened rhythm from the first chart, produced in one night.
Evening cortisol is the part of the rhythm that matters most for stress eating, because it coincides with the hours when most stress eating happens, when willpower is depleted, and when the day's stressors have accumulated. It is also the part most associated with visceral fat. A person sleeping six hours, working under sustained pressure, and eating for relief at 9 pm has three inputs pushing the same direction, and the GLP-1 addresses only the third.
The first weeks on a GLP-1 can disturb sleep through nausea, reflux, waking to urinate, and, for a minority, vivid dreams or early waking. The sleep and circadian article on this site sets out the timing strategies that help. For cortisol specifically, the practical point is that a consistent wake time anchors the awakening response, and the awakening response anchors the rest of the curve. Protecting the first hour after waking, with light, a fixed time, and no scrolling in bed, does more for the daily rhythm than any supplement.
How Much Does One Bad Night Raise Evening Cortisol?
Percent increase in next evening plasma cortisol versus a normal night, in healthy young men, from Leproult et al 1997
Four hours in bed produced most of the effect of a full night without sleep. The elevation was concentrated between 4 pm and 9 pm, which is also the window in which most stress eating occurs. This was a small laboratory study in young men; the direction has been replicated many times, the exact magnitudes vary.
Does exercise raise or lower cortisol?
Both, and the intensity decides which
Exercise raises cortisol during and shortly after a session and lowers baseline cortisol and stress reactivity over weeks of training, and the threshold for the acute rise sits at moderate intensity. Hill and colleagues had trained men exercise for 30 minutes at 40, 60, and 80 percent of maximal capacity on separate days. At 40 percent, cortisol did not rise at all; at 60 percent it rose meaningfully; at 80 percent it rose further. Below about 60 percent of capacity, which for most people is a brisk walk or an easy ride, the session is a net withdrawal from the stress axis rather than a deposit.
The acute rise is not a reason to avoid hard training. Cortisol during exercise mobilises fuel and is part of a normal adaptive response, and in regular exercisers both resting cortisol and the cortisol response to psychological stress fall over time. The problem arises when hard sessions are stacked onto sustained life stress, short sleep, and a large calorie deficit. In that setting the recovery capacity that would normally absorb the training stress is already spent, and the person ends up with a flattened rhythm, disturbed sleep, and stalled progress that looks like the drug not working.
On a GLP-1, where protein intake and total energy are both reduced, the practical balance leans toward resistance training at moderate loads for muscle preservation, as the muscle retention article on this site sets out, plus daily walking, with high intensity intervals limited to two or three sessions a week and dropped entirely in weeks when sleep is poor. The people who do best on these drugs over the long term are rarely the ones training hardest; they are the ones sleeping and recovering best.
What is worth doing about cortisol on a GLP-1 microdose?
Five adjustments, none of which are a protocol
Everything below is context for a conversation rather than an instruction. The trial figures apply to the approved products at labelled doses, and any low dose or compounded regimen needs its own assessment from the prescriber who wrote it.
A consistent wake time anchors the cortisol awakening response, and the awakening response anchors the rest of the curve. One night of four hours in bed raised evening cortisol by 37 percent in Leproult et al 1997. Protecting sleep in the first weeks, when nausea and reflux disturb it, is the highest yield change available.
When comfort food stops working, the stress it covered becomes visible. A flat or irritable few weeks after starting is common, is not depression, and is not a drug effect. Replacing the function the food served, with a walk, a call, or a conversation with a clinician, resolves it for most people.
Each escalation step is a fresh acute stimulus to the stomach and, on the animal data, to the stress axis, and nausea itself activates the same brainstem circuits that drive cortisol. A dose held steady at a low level meets that stimulus once. Progress that is slower and calmer is progress the stress axis can absorb.
Restricting to 1,200 kcal a day raised cortisol output and tracking calories raised perceived stress in Tomiyama et al 2010. A GLP-1 delivers the deficit through appetite, which removes the tracking; a low dose keeps the deficit in the range that does not read as famine. Aim for 0.5 to 1 percent of body weight a week, not more.
Exercise below about 60 percent of maximal capacity did not raise cortisol in Hill et al 2008, and regular training lowers baseline cortisol over time. Daily walking and resistance work at moderate loads protect muscle and lower the evening floor. High intensity sessions are fine at two or three a week and worth skipping in weeks when sleep is short.
What is genuinely unresolved here?
Three gaps worth naming
No published study has measured cortisol rhythms, the awakening response, or stress reactivity in people taking semaglutide or tirzepatide at any dose. The acute stimulation data come from rodents and from an exendin-4 infusion in healthy volunteers, and the habituation data come from rodents alone. The inference that a weekly subcutaneous drug at a low dose produces a smaller and briefer stimulus than an intravenous infusion of a short acting agonist is pharmacologically reasonable but untested. The absence of a cortisol excess signature in the long trials is reassuring, and it is still an absence rather than a measurement.
The control of eating data from STEP 5 come from a questionnaire completed by trial participants at the full 2.4 mg dose. Whether a low dose produces the same improvement in craving control, a smaller one, or a threshold effect that only appears above a certain exposure is not known, because no trial has asked. The people on this site's low dose protocols who describe reduced stress eating are reporting a real experience, and it remains an unmeasured one. The same applies to the mood data: the reassuring trial and database findings describe labelled doses, and low dose protocols have not been studied for psychiatric outcomes at all.
The individual differences are large and poorly predicted. High cortisol reactors in the Epel studies were a minority of participants, and the people most likely to benefit from an intervention on the stress eating loop are the ones in whom the loop is most active, which is not something a standard clinical assessment captures. Waist to hip ratio, self reported emotional eating, and evening eating pattern are reasonable proxies. Salivary cortisol testing is available and is rarely worth the money for an individual, because single day values are noisy and the rhythm is what matters. The most reliable signal remains the person's own account of when, and why, they eat.
Frequently Asked Questions
Selected References
- Dallman MF, Pecoraro N, Akana SF, et al. Chronic stress and obesity: a new view of comfort food. Proceedings of the National Academy of Sciences, 2003. The cortisol and comfort food loop.
- Adam TC, Epel ES. Stress, eating and the reward system. Physiology and Behavior, 2007. Review of cortisol, reward, and palatable food intake.
- Epel E, Lapidus R, McEwen B, Brownell K. Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior. Psychoneuroendocrinology, 2001. High versus low cortisol reactors and food intake after stress.
- Epel ES, McEwen B, Seeman T, et al. Stress and body shape: stress-induced cortisol secretion is consistently greater among women with central fat. Psychosomatic Medicine, 2000.
- American Psychological Association. Stress in America: Are Teens Adopting Adults' Stress Habits? 2013 survey, stress and eating findings. The 38 percent stress eating figure and subgroups.
- Ghosal S, Myers B, Herman JP. Role of central glucagon-like peptide-1 in stress regulation. Physiology and Behavior, 2013. Central GLP-1 signalling, HPA activation, dose dependence, and habituation in rodents.
- Gil-Lozano M, Pérez-Tilve D, Alvarez-Crespo M, et al. GLP-1(7-36)-amide and exendin-4 stimulate the HPA axis in rodents and humans. Endocrinology, 2010. ACTH and cortisol response to exendin-4 infusion in healthy volunteers.
- Wharton S, Batterham RL, Bhatta M, et al. Two-year effect of semaglutide 2.4 mg on control of eating in adults with overweight/obesity: STEP 5. Obesity, 2023. Control of Eating Questionnaire domains at weeks 20, 52, and 104.
- Wang W, Volkow ND, Berger NA, Davis PB, Kaelber DC, Xu R. Association of semaglutide with risk of suicidal ideation in a real-world cohort. Nature Medicine, 2024. Hazard ratios for first-time and recurrent suicidal ideation.
- US Food and Drug Administration. FDA Drug Safety Communication: update on FDA's ongoing evaluation of reports of suicidal thoughts or actions in patients taking a certain type of medicines approved for type 2 diabetes and obesity. January 2024.
- Tomiyama AJ, Mann T, Vinas D, Hunger JM, DeJager J, Taylor SE. Low calorie dieting increases cortisol. Psychosomatic Medicine, 2010. Restriction raised cortisol output; monitoring raised perceived stress.
- Leproult R, Copinschi G, Buxton O, Van Cauter E. Sleep loss results in an elevation of cortisol levels the next evening. Sleep, 1997. The 37 and 45 percent evening cortisol increases.
- Clow A, Thorn L, Evans P, Hucklebridge F. The awakening cortisol response: methodological issues and significance. Stress, 2004. Size and timing of the awakening response.
- Hill EE, Zack E, Battaglini C, Viru M, Viru A, Hackney AC. Exercise and circulating cortisol levels: the intensity threshold effect. Journal of Endocrinological Investigation, 2008. Cortisol response at 40, 60, and 80 percent of maximal capacity.
- Rebuffé-Scrive M, Lundholm K, Björntorp P. Glucocorticoid hormone binding to human adipose tissue. European Journal of Clinical Investigation, 1985. Glucocorticoid receptor density in visceral versus subcutaneous fat.
- Wilding JPH, Batterham RL, Calanna S, et al. Once-weekly semaglutide in adults with overweight or obesity (STEP 1). New England Journal of Medicine, 2021. Weight loss, nausea rates, and psychiatric adverse events.
- Novo Nordisk. Wegovy (semaglutide) injection, US prescribing information. Section 2, dose escalation schedule.
This article is for general educational purposes only and does not constitute medical advice, diagnosis, treatment, or a recommendation to start, stop, switch, or change the dose of any medication, supplement, exercise programme, or dietary habit. Semaglutide, tirzepatide, and all other GLP-1 receptor agonists are prescription medicines, and the choice of product, dose, and any low dose or microdosing approach should be decided and monitored by a qualified healthcare provider. The cortisol figures quoted here come from laboratory studies of stress, sleep, diet, and exercise in people not taking a GLP-1; cortisol rhythms have not been measured in people taking these medicines, and the diurnal and awakening response curves are illustrations of published reference ranges rather than measurements from GLP-1 users. The low dose schedule shown is illustrative and has not been tested in clinical trials. Nothing here is intended to diagnose, prevent, treat, or cure obesity, Cushing's syndrome, adrenal insufficiency, depression, anxiety, an eating disorder, insomnia, or any other condition, and no low dose or microdosing approach described in this article has been shown in trials to be safe or effective outside the specific trial conditions cited. Anyone experiencing persistent low mood, thoughts of self harm, binge eating, purging, or severe anxiety should contact a healthcare provider promptly; in the United States, the 988 Suicide and Crisis Lifeline is available by call or text. Individual results vary.
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