Are You Losing Weight Due To Stress? Here’s What To Do

Chronic stress can cause unexplained weight loss. Stress can affect the brain function, heart health, behavior, internal organs, and immunity . Chronic stress can also cause tumor development.

Hence, it is important that you listen to your body’s response to chronic stress. If you are losing weight and are constantly under stress, this post is for you. Here, you will learn how to reduce stress and prevent unnatural weight loss. Keep reading!

How Does Stress Cause Weight Loss?

Here are the various ways chronic stress causes weight loss:

  • Produces Stress Hormones

When you are under constant stress, your body is constantly in the flight or fight mode. This means that you are always producing the stress hormones, adrenaline and cortisol. These hormones affect your digestion, immunity, and sleep patterns.

Adrenalin works by preparing your body for vigorous physical activity, but it also reduces your appetite. Cortisol acts by suppressing certain body functions that are unnecessary during stressful situations, like the reproductive function, digestion, and immunity.

  • Affects Hunger And Digestion

Due to the dual hormonal effect on your body, you might not feel hungry often or at all. It affects your vagus nerve (the nerve that is responsible for GI tract peristalsis or movement of digested food through your gastrointestinal tract), which also affects digestion and absorption of food. Your digestive system will malfunction, and you might end up with diarrhea and GI tract inflammation.

  • Burns Calories

Under stress, you can also burn extra calories by nervously moving some part of your body – like tapping your feet or clicking your fingers. You might feel the need to get rid of the stress by working out and end up overexercising. This can also lead to unwanted weight loss.

  • Affects Sleep

Stress can also affect your sleep patterns. It can be tough to fall asleep and equally tough to stay asleep. Disrupted sleep can make you feel sluggish and fatigued all the time. And that, in turn, can produce more cortisol.

Now it makes sense why you are losing all that weight, right? But there’s one more thing you must know. Scroll down to find out.

Anxiety Causes Weight Loss

Forty million American adults are affected by anxiety. And anxiety can also be triggered by chronic stress. The stress hormones, adrenaline and cortisol, get triggered when you are super anxious, thereby opening the gateway for more stress.

Did You Know?

  • Anxiety disorders are the most common mental illness in the U.S., affecting 40 million adults in the United States age 18 and older, or 18.1% of the population every year.
  • Anxiety disorders are highly treatable, yet only 36.9% of those suffering receive treatment.
  • People with an anxiety disorder are three to five times more likely to go to the doctor and six times more likely to be hospitalized for psychiatric disorders than those who do not suffer from anxiety disorders.
  • Anxiety disorders develop from a complex set of risk factors, including genetics, brain chemistry, personality, and life events.

Anxiety and Depression

It’s not uncommon for someone with an anxiety disorder to also suffer from depression or vice versa. Nearly one-half of those diagnosed with depression are also diagnosed with an anxiety disorder.

If you have ever paced up and down, felt a dull pain in your chest, bitten your nails without even realizing it, or got up in the middle of the night drenched in sweat, you know what I am talking about.

Anxiety and stress go hand in hand. It always helps to be aware of the triggers that cause you to become anxious and stressed out. We will discuss what to do when you are stressed out in a bit. Let’s first check out some more symptoms so that it is easy for you to understand if you are losing weight due to stress.

Symptoms Of Weight Loss Due To Stress

  • Fatigue
  • Difficulty falling asleep
  • Indigestion
  • Body ache
  • Tense neck muscles
  • Frequent mood swings
  • Palpitation
  • Decreased sex drive
  • Slowed brain function
  • Loss of appetite
  • Need to do a task obsessively and repeatedly
  • Biting nails or lips
  • Tapping feet
  • Dilated pupils

If you display more than one of these symptoms, we can help you. Try the following ways to reduce stress and prevent unexplained weight loss.

10 Tips To Control Weight Loss Due To Stress

1. Identify The Trigger

The first step to reducing stress is accepting that you are under stress and identifying the triggers. Is it work? Your relationship? Finances? A memory? Once you acknowledge what is causing you to get stressed, you will be in a better position to address the problem.

2. Breathe!

You will save a lot of time and energy just by focusing on your breathing. Close your eyes softly and start breathing in slowly. Feel the cold air entering your nostrils and into your windpipe. Count 1-5 and exhale slowly. Feel your chest moving down and the chest pain reducing a little. Do this 10 times every time you know that you are stressed out. You will feel calmer immediately.

3. Write Down How You Feel

The next step is to acknowledge your feelings. Are you feeling hurt? Angry? Hatred? Worried? Well, write them all down. Write what or who is causing you to get so stressed. Just like talking to a friend, your journal can help you vent out the negative emotions from your system. Do it, and you will feel lighter.

4. Seek Help

Life will throw lemons, and you will learn how to make lemonade. But, sometimes, the lemonade can turn bitter if you are not careful. My point is, you cannot do everything alone. It’s OK to seek help when you need it. Your strength lies in giving your body and soul the relief that they deserve. Talk to a professional or a friend. Slowly, you will start to develop a third perspective that will make the whole “stress situation” clear. It is going to help you take the burden off your shoulders.

5. Eat In Small Quantities

You might not feel hungry at all, we understand. That’s why we recommend you consume small quantities of food. It is going to be tough taking even a bite, but trust the process. Equip yourself to get back up, find your ground, and stay put. For that, you need a human being’s basic need – food! Eat just a little or make a juice or smoothie and drink it. You will slowly start getting back to your normal food habits.

6. Post-Workout Nutrition Is A Must

If you work out regularly and have been working out even more to get rid of stress, you must start drinking a post-workout smoothie to prevent unwanted weight loss. A post-workout drink will help replenish the electrolytes, proteins, and carbs that your body needs to recover from the workout. Start with a small quantity and then get to drinking a tall glass of a post-workout smoothie.

7. Start Learning A New Skill

Learning a new skill can help reduce stress. Learn what you always wanted to because there’s no better time than NOW. Learning stimulates the brain and keeps it occupied. You will also meet new people and develop a different outlook on life.

8. Make New Professional Connections

Work and professional life can be stressful. Make new professional connections, not necessarily from the same field. Sometimes, it is from various kinds of discussions that you might bump into a great idea that you can actually implement and that would show great results. Talking about something totally different from your profession can help you widen your professional network as well as your ability to think beyond what you already know.

9. Hydrate

Drink water and freshly pressed juices. Hydration is as important as food. Drinking water or juice will help flush out the toxic build-up and restore your body and brain functions. Add some mint leaves and cucumber slices to add a punch to the water. You will definitely start feeling better in no time.

10. Compartmentalize

One of the most important points to deal with stress is learning how to compartmentalize. This means, you know when you think about what. If you have a dwelling problem at your workplace and come home thinking about it, you will not be able to enjoy your time with your family or yourself. Yes, it can be difficult to do and will need practice. Try writing down what you need to do for the day and check those boxes when you finish those tasks. That way, you will remain focused on your work or on spending time with family.

Stress has become an integral part of our lives. But it doesn’t really have to be. The choice is yours – whether you want to reduce stress and enjoy life or dwell in thoughts and emotions that do no good for you or anyone. Choose the former because you deserve to experience all the joys and wonders life has to offer. Write to us if you think this post is helpful. And don’t forget to BREATHE! Take care.

The effects of chronic stress on health: new insights into the molecular mechanisms of brain–body communication

Today’s life rhythms and demands are often challenging and require intense physical and psychological efforts in order to be sustained. An individual reacts to physical and mental strain that is potentially health threatening by activating interconnected neuroendocrine circuits. This response allows the body to face and deal with the challenge and re-establish homeostatic equilibrium. If the individual perceives a noxious stimulus as too intense, or its duration as too long, he may fail coping with it, and incur maladaptation. In this case, the stress response does not resolve into a state of balance (either similar or new, i.e., adapted, compared with the state before stress hits), neuroendocrine parameters remain altered, and illness may ensue.

It is clear that stress has both a physical (objective) and a psychological (subjective) component: the latter, as described by Koolhaas and colleagues, depends on the individual perception of its predictability and controllability. The way a person can anticipate a certain stressor and then control it, largely defines the resulting stress response, how promptly and efficiently it is activated promoting adaptation, and how fast it is turned off once equilibrium has been recovered.

The time course of the stress response, characterized by measurable neuroendocrine and behavioral indexes, thus reveals whether a destabilizing stimulus is manageable, or conversely, cannot be handled and consequently becomes harmful.

This implies that not all stimuli that elicit strong neuroendocrine responses are real stressors, but only those that exceed the individual’s ability to change and adapt.

Cortical centers in the brain sense a disturbing stimulus and respond by activating pathways that through the limbic system stimulate peripheral networks, including the sympathetic–adrenal–medullary axis and the renin-angiotensin system, and later the hypothalamic–pituitary–adrenal (HPA) axis. A cascade of events follows that results in the orchestration of a complex response. Adrenaline and other hormones, and neuropeptides are produced and regulate cardiovascular and metabolic functions (inducing, for instance, increases in heart rate, breath frequency, glucose release) for a prompt response concerted to overcome the challenge.

If the distressing stimulus persists, the HPA axis kicks in to sustain the immediate reaction mediated by the centrally activated peripheral systems. The HPA response starts with the hypothalamus delivering corticotropin-releasing hormone to the pituitary and culminates with the stimulation of the adrenal cortex by the pituitary-derived adrenocorticotropic hormone to produce glucocorticoids (GCs). Most organs and tissues, including sympathetic nerves, immune cells and several brain regions express GC receptors and are responsive to GCs induced by stress. Consequently, these hormones participate in the regulation of disparate stress-associated processes, from the modulation of cardiovascular effects and the immune function, to the eventual dampening of the stress response through inhibition of the HPA axis when adaptation is attained.

In situations in which the stressor is overwhelming and cannot be resolved, stress becomes chronic. In this case, the GC-dependent negative feedback mechanism that controls the stress response does not work, GC receptor resistance develops, and the systemic levels of the molecular mediators of stress remain high, compromising the immune system and damaging in the long-term multiple organs and tissues.

What is the actual impact of chronic stress on health?

When considering the numerous cellular targets of the chemical mediators of stress, one would expect that protracted, stress-dependent neuroendocrine dysregulation may damage directly or through functional circuits practically all organs and tissues. To clarify this assumption and identify the biochemical pathways significantly impaired by chronic stress to the extent of producing illness, researchers have on one hand searched for putative morphological tissue alterations associated with stress, and on the other analyzed the molecular mechanisms of action of the main stress hormones.

Effects of chronic stress on brain structure

It has been shown that chronic stress is linked to macroscopic changes in certain brain areas, consisting of volume variations and physical modifications of neuronal networks. For example, several studies in animals have described stress-related effects in the prefrontal cortex (PFC) and limbic system, characterized by volume reductions of some structures, and changes in neuronal plasticity due to dendritic atrophy and decreased spine density. These morphological alterations are similar to those found in the brains of depressed patients examined postmortem, suggesting that they could also be at the basis of the depressive disorders that are often associated with chronic stress in humans. This hypothesis is supported by imaging studies that evidenced structural changes in the brain of individuals suffering from various types of stress-related disorders, such as those linked to severe traumas, major negative life events or chronic psychosocial strain. In particular, Blix and colleagues observed atrophy of the basal ganglia and significantly reduced gray matter in certain areas of the PFC in subjects afflicted with long-term occupational stress. In general, the consequences of these alterations in a brain region can expand to other functionally connected areas, and potentially cause those cognitive, emotional and behavioral dysfunctions that are commonly associated with chronic stress, and that may increase vulnerability to psychiatric disorders.

Interlink between the brain & the immune system

The understanding of the molecular circuits that underlie brain architectural changes and medical conditions linked to chronic stress is just at the beginning. Research in this area has centered primarily on the signaling functions of those molecules that are directly induced by stress through the activation of the sympathetic-adrenal-medullary and HPA networks, focusing on their possible cellular targets. Since receptors for stress neuropeptides and hormones are broadly expressed in immune cells, most studies have concentrated on the effects of stress on the immune system (IS). In fact, psychological stress can induce the acute phase response commonly associated with infections and tissue damage, and increase the levels of circulating cytokines and of various biomarkers of inflammation. As suggested by Maier and Watkins, the interlink between the stress response and inflammation elicited by the IS can be explained from the evolutionary perspective by considering that the stress response is an adaptive process developed by co-opting the IS mechanisms of defense. In this frame, a psychological stressor, perceived by the brain as ‘danger’, that is, potentially harming, sets in motion a neuroimmune circuit that stimulates the IS to mount a protective reaction intended to prevent damage, repair it and restore homeostasis.

This neuroimmune communication is bidirectional because the cytokines produced by stress-stimulated immune cells also convey a feedback to the nervous system, further modulating the release of stress hormones in the brain, as well as brain activity that regulates behavior and cognitive functions. In a situation of chronic stress, the neuroimmune axis can be overstimulated and breaks down, thus causing neuroendocrine/immune imbalances that establish a state of chronic low-grade inflammation, a possible prelude to various illnesses.

Diseases whose development has been linked to both stress and inflammation include cardiovascular dysfunctions, diabetes, cancer, autoimmune syndromes and mental illnesses such as depression and anxiety disorders.

Persistent, abnormal levels of cytokines and stress chemical mediators in the brain may also damage the parenchyma and cause neuronal death, thus contributing to the brain structural changes associated with chronic stress that are described above.

Despite the large number of studies that have addressed the biological effects of chronic stress and their impact on human health, the emerging picture still merely outlines the biochemical and functional responses of the nervous and immune systems to long-term stress, highlighting some nodes of information exchange between the two networks, but still lacking essential elements concerning additional cellular players, and functional and molecular mechanisms.

Some recent studies have, however, significantly improved our knowledge of how chronic stress promotes two of the diseases that have long been associated with it: atherosclerosis and depression.

Effects of chronic stress on hematopoietic stem cells in cardiovascular diseases

Heidt and colleagues demonstrated how stress increases the levels of circulating inflammatory leukocytes by direct stimulation of hematopoietic stem cell proliferation. In this new pathway, stress induces the release of noradrenaline by sympathetic nerve fibers targeting blood vessels in the bone marrow of mice. The catecholamine then acts on mesenchymal stem cells located in the hematopoietic niche, which express high levels of the β3 adrenergic receptors. One of the consequences of this interaction is the downregulation of the chemokine CXCL12, a known target of noradrenaline, which is normally produced by several types of niche cells, including mesenchymal stem cells. This releases the inhibition typically exerted by CXCL12 on the proliferation of hematopoietic stem and progenitor cells and on leukocyte migration, thus promoting cell division and leukocyte mobilization into the bloodstream.

Predictably, the inflammatory response induced by the activation of this neuroimmune pathway may have adverse health effects, in particular by exacerbating pre-existing medical conditions. Specifically, the study demonstrated that this mechanism became activated when atherosclerosis-prone mice ApoE-/- were subjected to long-term stress, leading to enhanced recruitment of inflammatory cells in atherosclerotic plaques, higher levels of proteases and increased plaque fragility. Most interestingly, β3-adrenergic receptor blockers opposed leukocyte production and mobilization, thus counteracting plaque inflammation.

When shifting their attention to human subjects, the scientists determined that individuals under considerable occupational stress had significantly more circulating leukocytes compared with when they were not working, suggesting that the neuroimmune mechanism they discovered might be set off by chronic stress and sustain an inflammatory reaction also in humans. If demonstrated, this would open the way to conceptually new therapeutic possibilities not only for atherosclerosis and its related complications, but also for other stress-related diseases that are aggravated by chronic inflammation.

Mechanisms of chronic stress-associated depression & brain–skeletal muscle communication

The mechanisms by which stress chemicals may induce depression are mostly undetermined. Research in this field is starting to define how multiple, independent, though often interconnected biochemical pathways affected by chronic stress concur to promote this disease.

Ota and colleagues have identified a molecular mechanism triggered by chronic stress that contributes to neuronal atrophy in specific brain areas, an anomaly that is typically observed in depressed patients, independent of the cause of depression. In their study, they observed that persistent high levels of GCs, resulting from stress-induced hyperactivation of the HPA axis, stimulate the production of the molecule REDD1 in the PFC of rodents subjected to prolonged stress. REDD1 is generally induced by a variety of stressors – from energy stress, to hypoxia, to DNA damage – in most tissues and inhibits the kinase mTORC1, thus altering the phosphorylation state and function of its targets. In the brain, the interference of REDD1 with mTORC1 signaling ultimately impinges on neuronal protein synthesis, spine formation and synaptic plasticity. The inhibition of mTORC is pivotal for synaptic impairment and appears to be a central endpoint of molecular pathways turned on by chronic stress. In fact, also the decrease of brain-derived neurotrophic factor levels in response to chronic stress disrupts mTORC1 function.

Proinflammatory cytokines induced by stress are also involved in the development of chronic stress-associated depression. The acute phase response generally triggered by a harmful factor implies the so-called sickness behavior that includes symptoms similar to those typical of depressive disorders, like social withdrawal, decreased physical activity, fatigue, somnolence, mood and cognitive alterations. This adaptive response is orchestrated by cytokines, and is meant to divert an individual from normal activities in order to save energy, thus facilitating a reaction against the challenge, and subsequent recovery. In the case of chronic inflammation that may set in with prolonged stress, persisting cytokine signaling in the brain prevents the resolution of sickness behavior that consequently can degenerate into depression. The biochemical mechanisms underlying cytokine-induced depression are not well defined, but they may involve alterations of serotonin and glutamatergic transmission, and induction of GC resistance.

One of the pathways that are implicated drives the oxidation of tryptophan (a precursor of serotonin) to Kynurenin (Kyn) and results in the brain production of several neuroactive molecules. The enzymes tryptophan 2,3-dioxygenase and indoleamine 2,3-dioxygenase trigger the Kyn pathway in the liver and extrahepatically respectively, and can both be activated by chronic stress: tryptophan 2,3-dioxygenase in fact responds to GCs, while indoleamine 2,3-dioxygenase is induced by proinflammatory cytokines. The Kyn pathway not only affects the brain levels of serotonin and thus serotonergic transmission and its mood and behavioral effects, but it is also responsible for the production of tryptophan metabolites that have neuroinflammatory properties or can affect glutamatergic neurotransmission in the brain either positively or negatively. It follows that a shift in the pathway that favors the production of 3-hydroxykynurenine – an inducer of reactive oxygen species and inflammation – and quinolinic acid – an N-methyl-d-aspartate receptor agonist – over the antioxidant and N-methyl-d-aspartate receptor inhibitor kynurenic acid, may promote depression.