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Some Symptoms Seem To Have A Seasonal Trend


Chaos

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I'm curious if any one else has noticed any kind of seasonal pattern to any of your dysautonomia type symptoms? For example, my GI symptoms are always much worse from about this time of year until the end of June. It starts with February as nausea month, then add in March which has been esophageal pain month, April adds in terrible diarrhea and intestinal pain , May is odd rashes, hives, angioedema and esophageal spasm- in- addition- to-all- the- other -GI- symptoms (nausea, intermittent constipation...you know the drill) month. I've started calling it my "seasonal affected gut syndrome" or SAGS for short. :( My GI doctor just looks at me and shakes his head when I tell him this, but then when he looked back at my records he had to admit that he had ordered an abdominal US nearly every March for the past 5 years. (etc. etc.) I have GI symptoms during the rest of the year too, but never as bad or as consistently bad as during the spring.

For those of you with MCAD would any of these complaints go along with some type of MCAD? I do have seasonal allergies which are worst in the spring and fall.

I started noticing the pattern after reading an article by a DOM (doctor of Oriental Medicine) who said GI symptoms were worse in the spring due to the "liver having a hard time with the change from winter to spring." Since I was having a lot of GI issues at the time, and it was spring, I thought I'd watch to see and for the past 5 years it has certainly been true for me at least. Now I'm wondering if there's a more scientific explanation than my liver having issues with the change of seasons. :) If you all don't come up with something good, I guess I'll stick with the lazy liver theory! ; )

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For those of you with MCAD would any of these complaints go along with some type of MCAD? I do have seasonal allergies which are worst in the spring and fall.

Hello Chaos,

Without a doubt my ANS stuff is worse when my environmental intolerance is worse, which tends to start with the tree pollen season, then other pollens in late Jan early Feb, through to mid Sept. I have noticed that my children's ANS symptoms are also more noticeable then too. Interestingly my children's gut issues are also much worse if they have a virus. The minute they get a bug they have extra bad acid reflux that Omeprazole does not touch and they down Gaviscon like it was water!! When one of my boys was on steroids and antihistamines for nasal polyps he oddly had less ANS symptoms.

Anna

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My allergies are also tied to my POTS. Every year, I would think that the kids brought home the "latest bug" because I would get sick as soon as school started. After being skin tested for allergies, it turned out to be an almost anaphylactic reaction to ragweed pollen. Last year, I saw an allergist regularly and did not get my yearly sinus infection.

As for another theory, it could be light related (like SAD.) The lower levels of light in the winter can trigger seasonal depression and can certainly mess with the hormones and neurochemicals in the brain. Since most serotonin is produced in the gut, your fix could be as simple as getting a light box. It could also be vitamin D deficiency due to covering up and not getting as much sun exposure.

It could be a liver issue, but if it is, there has got to be an unexplained reason for it. Many diseases wax and wane with menstrual cycles as well as seasons, why not liver function? There can be great truth in "alternative" medicine, especially with thousands of years of observation behind it. "Modern" medicine is simply putting the old observations under a microscope and taking its best shot at explaining it with the information they know at the time.

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CNS Drugs. 2009;23 Suppl 2:3-13. doi: 10.2165/11318620-000000000-00000.

Neurobiology of circadian systems.

Schulz P, Steimer T.

D?partement APSI, H?pitaux Universitaires de Gen?ve et Facult? de M?decine de Gen?ve, 1225 Ch?ne-Bourg, Switzerland. pierre.schulz@hcuge.ch

Time is a dimension tightly associated with the biology of living species. There are cycles of varied lengths in biological activities, from very short (ultradian) rhythms to rhythms with a period of approximately one day (circadian) and rhythms with longer cycles, of a week, a month, a season, or even longer. These rhythms are generated by endogenous biological clocks, i.e. time-keeping structures, rather than being passive reactions to external fluctuations. In mammals, the suprachiasmatic nucleus (SCN) is the major pacemaker. The pineal gland, which secretes melatonin, is the major pacemaker in other phyla. There also exist biological clocks generating circadian rhythms in peripheral tissues, for example the liver. A series of clock genes generates the rhythm through positive and negative feedback effect of proteins on their own synthesis, and this system oscillates with a circadian period. External factors serve as indicators of the astronomical (solar) time and are called zeitgebers, literally time-givers. Light is the major zeitgeber, which resets daily the SCN circadian clock. In the absence of zeitgebers, the circadian rhythm is said to be free running; it has a period that differs from 24 hours. The SCN, together with peripheral clocks, enables a time-related homeostasis, which can become disorganized in its regulation by external factors (light, social activities, food intake), in the coordination and relative phase position of rhythms, or in other ways. Disturbances of rhythms are found in everyday life (jet lag, shift work), in sleep disorders, and in several psychiatric disorders including affective disorders. As almost all physiological and behavioural functions in humans occur on a rhythmic basis, the possibility that advances, delays or desynchronization of circadian rhythms might participate in neurological and psychiatric disorders has been a theme of research. In affective disorders, a decreased circadian amplitude of several rhythms as well as a phase advance or delay have been described, leading to hypotheses about changes in biological clocks themselves or in their sensitivity to environmental factors, such as light or social cues. Molecular genetics studies have suggested the involvement of circadian clock genes, but no tight association has yet been found. Agomelatine is an antidepressant, agonist at melatonergic MT(1), MT(2) receptors and antagonist at 5-HT(2C) receptors, and is able to phase advance circadian rhythms in humans. The fact that non-pharmacological (light therapy, sleep deprivation, rhythm therapy) and pharmacological (lithium, antidepressants, agomelatine) therapies of affective disorders influence circadian rhythms indicates that biological clocks play a role in the pathophysiology of these disorders.

PMID: 19708721

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