When PTSD comes up in clinical conversations, it’s usually framed as a disorder of memory, fear, and nervous system “stuckness.” All true.
But the more I read (and the more I work with clients impacted by trauma), the more I think this framing is incomplete.
This review paper makes the case that PTSD can be understood as a whole-body metabolic condition, not just a psychiatric diagnosis, with overlapping biology seen in metabolic syndrome (and related cardiometabolic outcomes). That shift matters to dietitians, therapists, and other healthcare professionals who want care plans that actually align with what’s happening physiologically.
Below, I’m breaking down the key mechanisms from the article Post-Traumatic Stress Disorder: A Metabolic Disorder in Disguise? and translating the science into practical, trauma-informed clinical takeaways.
Table of Contents
First, a quick clarity check: “trauma” vs PTSD
In real-world practice (and in trauma-informed care), we often talk about trauma more broadly than the DSM definition of PTSD.
- A person can have trauma-related symptoms (sleep disruption, hypervigilance, appetite changes, GI issues, emotional numbing, dissociation, panic) without meeting full PTSD criteria.
- PTSD, specifically, includes hallmark features like impaired fear inhibition, re-experiencing, avoidance, and hyperarousal, plus defined exposure criteria and duration.
Why do I bring this up? Because the physiology in this paper helps explain why even subthreshold PTSD symptoms can show up with very “metabolic-looking” patterns in the body.
The core idea of the paper: PTSD doesn’t stay in the brain
The authors highlight something many of us have observed clinically:
People with PTSD have higher rates of cardiometabolic concerns, and the overlap isn’t only behavioral (“they eat worse” or “they don’t exercise”). The paper lays out shared metabolic changes seen in PTSD and Metabolic Syndrome (MetS), specifically:
- the HPA axis (stress hormones)
- the sympathetic nervous system (fight/flight)
- metabolic hormones (leptin, insulin, NPY)
- inflammation (IL-6, CRP, TNFα)
On page 24, their Table 1 is basically the “at-a-glance” version of this overlap (PTSD vs metabolic syndrome side-by-side).
It’s important to realize that these different mechanisms can all overlap and interact. While discussed separately, the individual with unresolved trauma or metabolic syndrome is likely experiencing all of these at once.
Mechanism #1: HPA Axis and Cortisol Release
Here’s the nuance that’s easy to miss:
- In many studies, PTSD is linked with a blunted cortisol response to acute stress and stronger negative feedback (think: the system shuts cortisol down quickly).
- In metabolic syndrome, you more commonly see patterns consistent with higher cortisol release and weaker negative feedback (think: the system doesn’t turn itself off well).
At first glance, those look opposite.
Although the “how” is different between PTSD and MetS, the result is the same: unregulated inflammation that continues to cause a downward spiral of metabolic changes.
Mechanism #2: Increased Sympathetic Tone
PTSD is strongly associated with:
- higher sympathetic activation (higher heart rate, higher skin conductance)
- lower heart rate variability (HRV) (less parasympathetic “brake”)
- higher norepinephrine (NE) at baseline and in response to stress
And… individuals with metabolic syndrome show a very similar autonomic pattern (including elevated NE and reduced HRV).
Clinically, this helps explain why some clients feel their bodies are always braced: sleep is lighter, digestion is off, appetite cues are chaotic, blood sugar feels “reactive,” and caffeine sensitivity can be intense. (Not because they’re doing something wrong. Because their physiology is working overtime.)
Mechanism #3: Alteration in Metabolic Hormones
This is one of the most “dietitian-relevant” sections of the paper.
Leptin
The paper notes that higher leptin levels have been observed in PTSD (suggesting possible leptin resistance in some cases).
Animal data also suggest that leptin may support fear extinction, a finding that becomes particularly interesting when leptin signaling is impaired.
Neuropeptide Y (NPY)
NPY is tied to stress regulation and resilience. Higher NPY has been associated with resilience in some trauma-exposed groups. However, in PTSD, peripheral NPY is often lower than in individuals who have not experienced trauma.
Insulin and glucose response
The review summarizes evidence that PTSD is associated with insulin resistance patterns (including higher insulin response on glucose challenge in some studies).
My take as a clinician: this is a strong reminder that appetite changes after trauma aren’t just psychological. The appetite + craving shifts many clients describe can be downstream of stress signaling and hormone dynamics.
This is not a motivation issue.
Mechanism #4: Brain energy metabolism changes
The paper highlights PET findings in PTSD that suggest:
- Reduced glucose metabolism in regions involved in executive function and memory (including prefrontal areas and hippocampus in some studies)
- Increased glucose metabolism in the amygdala (threat detection)
I don’t use this to imply “PTSD is caused by low glucose,” obviously. I use it to validate why planning, follow-through, impulse control, and emotional regulation can feel harder when someone is triggered or chronically activated.
It also makes me think differently about nutrition care plans: if executive function is taxed, then complexity and rigidity are the enemy.
Mechanism #5: Inflammation may be the shared “bridge” between PTSD and metabolic disease
This is the throughline of the review.
The authors propose inflammation as a common mechanism linking:
- Sympathetic activation (NE can stimulate innate immune activity)
- HPA axis disruption
- Metabolic changes (including insulin resistance)
- PTSD symptom severity (CRP and cytokines correlating with symptoms in some studies)
Figure 1 (page 23) is their conceptual model: normal stress physiology includes cortisol helping regulate inflammation, but in the “pathology” model, sympathetic drive + impaired glucocorticoid-immune feedback allows inflammation to stay elevated, feeding into downstream metabolic effects.
Dietitian’s Tip (for clinicians):
When a client discloses trauma history, I assume stress physiology is part of the nutrition picture, even if their labs look “fine” today.I focus on stabilizing inputs (regular meals, enough protein + fiber, steady hydration, gentle blood sugar support) and reducing the need for the body to compensate (extreme restriction, long fasting windows, high caffeine reliance, chaotic eating).
Simple, predictable nutrition can be a nervous-system intervention.
What This Means in Practice
Trauma-informed “metabolic care” (without turning nutrition into another stressor)
Here are the care principles I’d want dietitians and therapists to take from this paper:
1) Screen wider than food
If you’re a dietitian, it’s reasonable to ask about:
- Sleep quality
- Caffeine, alcohol, and substance use patterns
- GI function (especially stress-linked symptoms)
- Food access and safety
- Medication changes that can impact glucose/lipids/BP
If you’re a therapist, it’s reasonable to ask:
- “How does eating feel in your body lately?”
- “Do you notice appetite changes after triggers?”
- “Are there times of day when food feels impossible?”
…and refer to nutrition support early, not as a last resort.
If you’re a doctor, consider saying/asking:
- Do you have enough food to eat?
- Pick one small thing you can start today. You can add on more later.
- I would like to refer you to a dietitian/therapist/etc. Is that okay?
2) Build plans that work with a taxed nervous system
In PTSD physiology, the “cost” of decision-making can be high. So I lean on:
- repeatable meals/snacks
- predictable grocery lists
- low-cook or no-cook options
- consent-based tracking that emphasizes mindfulness (only if it helps; never as punishment or obligation)
3) Prioritize metabolic stability over dietary perfection
This paper supports a whole-body view of PTSD. So instead of chasing an idealized diet pattern, I’m looking for:
- fewer long gaps between meals (when possible)
- steady carbohydrate quality (not elimination)
- anti-inflammatory building blocks (fiber, omega-3 sources, colorful plants, adequate protein)
- realistic routines clients can maintain during flare-ups
4) Collaborate across disciplines
The review discusses the therapeutic implications of targeting shared systems (HPA axis, SNS, inflammation), including evidence supporting benefits from some cardiometabolic medications (ACE inhibitors/ARBs) and behavioral therapies.
As clinicians, we don’t have to “own” every intervention. We just need to stop treating PTSD like it has no body.
Limitations (and what I want more research on)
The authors are clear that a lot of this evidence is cross-sectional and heterogeneous. A few gaps that matter clinically:
- Directionality isn’t fully established: does PTSD drive metabolic changes, do pre-existing metabolic/inflammatory patterns increase PTSD risk, or both?
- Population bias: PTSD research often over-represents military samples; civilian trauma, chronic oppression-related trauma, and poverty-related trauma deserve more direct study. (This is something I keep coming back to clinically.)
- Sex differences: The paper flags this as important, and I agree, especially given known differences in PTSD prevalence and metabolic responses.
Bottom line
This paper supports a reframe I think many of us are ready for:
PTSD is not “just psychological,” and metabolic disruption is not “just lifestyle.”
The overlap runs through stress physiology, inflammation, autonomic regulation, and metabolic hormones.
And for our professions, the implication is simple:
If PTSD is a whole-body condition, then whole-body care, including nutrition support, belongs in the treatment plan, not on the sidelines.
