Several new readers posting here are trending to indicate alcohol as a major trigger for their afib. Weve discussed this in the past but perhaps it would serve bring this forward again.
I battled hypoglycemia for years and also had adrenal burnout. My first bout of AF came after several glasses of red wine. It could have been other impurities in the wine, but most likely, it was a hypoglycemic effect after the alcohol consumption as it accompanied several pieces of high-carb pizza. I have since given up gluten-containing grains such as wheat and wheat products. I also gave up all forms of alcohol. Now that Ive had an ablation, I may occasionally have a glass of wine or beer but I have lost the desire or need to indulge in alcohol on a regular basis.
What I learned about hypoglycemia and afib is that one should always eat a complete meal or snack
not just simple carbs. By complete, I mean adequate lean protein and a healthy fat along with a minor amount of non-starchy carbohydrate like non-starchy veggies (no French fries).
Never skip meals especially breakfast. Youve been without food for however long you were sleeping and the body needs to begin with a balanced breakfast for proper energy. Breakfast doesnt have to be breakfast food. Most of us have learned to eat other foods for breakfast.
The word breakfast means literally break the fast. Its the most important meal of the day. You cant go all night, run on empty for much of the day and expect your body to function well without adequate and proper fuel. If your day is stressful, it just magnifies the insult.
Eliminate all sugar, sugar-containing foods, sodas no diet, either and use fruit sparingly until the adrenals have been restored to proper function. This can take years to accomplish depending on the extent and duration of stress that brought about the adrenal fatigue.
Never go longer than 4 hours between a meal or a balanced snack.
If your evening meal is at 6 pm, then you are going to have to eat a small snack again 3 4 hours later but enough time before bed so the food can be digested and at least some of it pass through the stomach.
Hydrate well and often.
Keep in mind that when sugar-like substances are taken in, the body must then call for insulin to metabolize. Insulin uses potassium. Sugar depletes magnesium. Both electrolytes are essential to normal sinus rhythm (NSR). Most people are deficient in magnesium; and probably most are also deficient in adequate potassium.
Small wonder when we drink a lot of alcohol or alcohol on an empty stomach, that the reactive hypoglycemia sets in so quickly. This isnt the case for every individual, but is a very typical scenario as anyone working in the ER will tell you based on the recitations from those who rush to the ER with palpitations or outright afib after indulging to excess.
This is overly simplistic. There are many good books on hypoglycemia. Much of the information relating to hypoglycemia is found in that which relates to diabetes. Hypoglycemia can be a precursor to a diabetic condition later on.
Here are some clips from my files when I began looking into hypoglycemia many years ago.
Jackie
24-Apr-96 15:54:18
Sb: Understanding HG Lesson1
Fm: Barrett Chapin, MD
Handy bit of explanation as to alcohol and reactive hypoglycemia
There are 4 types of true reactive hypoglycemia. They are:
1) from early NIDDM (type II diabetes) or glucose intolerence
2) alimentary hypoglycemia
3) alcohol induced and
4) idiopathic "unknown cause"
Alcohol can cause FASTING hypoglycemia when alcoholics who have damaged their liver from years of alcohol abuse don't eat for a prolonged period.
Nonalcoholics can get REACTIVE hypoglycemia from drinking alcohol and eating carbohydrate. Alcohol can cause an excessive release of insulin when taken with carbohydrate. The excess insulin can lead to you know what. Yes, hypoglycemia!
The most common scenerio is when drinking alcohol and carbohydrate alone. It is said that a gin (alcohol) and tonic (pure carbohydrate) and a 50 gram biscuit (more carbohydrate) is a very effective stimulous for hypoglycemia (kids, don't try this at home). So if reactive hypoglycemia is your problem, cut out the alcohol.
Alcohol can also cause low blood sugar. It's best to talk to your doctor about alcohol.
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Causes of Hypoglycemia
In people taking certain blood-glucose lowering medications, blood glucose can fall too low for a number of reasons:
meals or snacks that are too small, delayed, or skipped
excessive doses of insulin or some diabetes medications, including sulfonylureas and meglitinides (Alpha-glucosidase inhibitors, biguanides, and thiazolidinediones alone should not cause hypoglycemia but can when used with other diabetes medicines.)
increased activity or exercise
excessive drinking of alcohol
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Diabetes Metab. 2000 Nov;26(5):337-51.
Postprandial reactive hypoglycemia.
Brun JF, Fedou C, Mercier J.
Service Central de Physiologie Clinique, Centre d'Exploration et de Readaptation des Anomalies Metaboliques et Musculaires (CERAMM), Lapeyronie Hospital Montpellier, France.
drjfbrun@aol.com
Postprandial reactive hypoglycemia (PRH) can be diagnosed if sympathetic and neuroglucopenic symptoms develop concurrently with low blood sugar (<3.3 mmol). Neither the oral glucose tolerance test (OGTT) nor mixed meals are suitable for this diagnosis, due to respectively false positive and false negative results. They should be replaced by ambulatory glycemic control or, as recently proposed, an hyperglucidic breakfast test.
PRH patients often suffer from an associated adrenergic hormone postprandial syndrome, with potential pathologic consequences such as cardiac arrhythmia.
PRH could result from (a) an exaggerated insulin response, either related to insulin resistance or to increased glucagon-like-peptide 1; (b) renal glycosuria; (c) defects in glucagon response; (d) high insulin sensitivity, probably the most frequent cause (50-70%), which is not adequately compensated by hypoinsulinemia and thus cannot be measured by indices of insulin sensitivity such as the homeostatic model assessment.
Such situations are frequent in very lean people, or after massive weight reduction, or in women with moderate lower body overweight. PRH is influenced by patient's alimentary habits (high carbohydrate-low fat diet, alcohol intake). Thus, diet remains the main treatment, although alpha-glucosidase inhibitors and some other drugs may be helpful.
PMID: 11119013 [PubMed - indexed for MEDLINE]
==================
[
diabetes.niddk.nih.gov]
Alcohol is high in calories and can cause hypoglycemia all by itself. Therefore, people with reactive hypoglycemia should avoid or limit alcohol.
[
www.gicare.com]
Gin and Tonic and Reactive Hypoglycemia: What Is
Importantthe Gin, the Tonic, or Both?*
DANIEL FLANAGAN, PETER WOOD, ROBERT SHERWIN, KWASI DEBRAH, AND
DAVID KERR
Metabolism Unit, Royal Bournemouth Hospital, Bournemouth, England; Endocrinology Laboratory,
Southampton General Hospital (P.W.), and the Division of Endocrinology, Yale University School of
Medicine (R.S.), New Haven, Connecticut 06520
[
jcem.endojournals.org]
ABSTRACT
The objectives of this study were to test the hypothesis that alcohol
can cause reactive hypoglycemia by attenuating the release of counterregulatory hormones.
The subjects were eight healthy volunteers five men and three women, aged 2040 yr). Each subject drank, using a randomized, double blind design 1) three large gin with regular tonics (0.5 g/kg alcohol and 60 g carbohydrate, mainly sucrose G1T); 2) the same amount of alcohol with Slim-line tonic (0.5 g carbohydrate; G alone); and 3) regular tonic without alcohol (T alone). Glucose, insulin, and counterregulatory hormone levels and middle cerebral artery velocity (MCAV), an index of cerebral blood flow, were measured.
Alcohol levels averaged 6070 mg/dL. Peak insulin levels were
similar in both studies in which regular tonic was consumed (95%
confidence interval for difference, 26 to 22 mU/mL). After the ingestion
of G1T, the blood glucose nadir was lower compared to that with
T alone (3.35 vs. 3.87 mmol/L; P , 0.02) or G alone (3.35 vs. 3.95
mmol/L; P , 0.01). After drinking gin, subjects reported typical hypoglycemic
warning symptoms unrelated to the prevailing glucose level. In both alcohol studies, there was marked blunting of GH release (P , 0.01). Despite a blood glucose nadir of 3.35 mmol/L, plasma epinephrine levels rose only slightly from 267 to 455 pmol/L (P 5 NS) after G1T. Ingestion of alcohol also caused a transient rise in right MCAV (P , 0.05) followed by a late drop in velocity in both cerebral hemispheres in the G1T study (P , 0.05)
In otherwise healthy individuals a combination of gin and regular
tonic can induce reactive hypoglycemia. Acute ingestion of alcohol
impairs the epinephrine response and markedly suppresses the release
of GH in response to a fall in blood glucose levels.
(J Clin Endocrinol Metab 83: 796800, 1998)
POSTPRANDIAL REACTIVE HYPOGLYCEMIA
J.F. BRUN, C. FEDOU, J. MERCIER
Diabetes & Metabolism (Paris) 2000, 26, 337-351
SUMMARY - Postprandial reactive hypoglycemia (PRH) can be diagnosed
if sympathetic and neuroglucopenic symptoms develop concurrently
with low blood sugar (<3.3 mmol). Neither the oral glucose tolerance
test (OGTT) nor mixed meals are suitable for this diagnosis, due to
respectively false positive and false negative results. They should be
replaced by ambulatory glycemic control or, as recently proposed, an
hyperglucidic breakfast test.
PRH patients often suffer from an associated adrenergic hormone postprandial syndrome, with potential pathologic consequences such as cardiac arrhythmia.
PRH could result from
(a) an exaggerated insulin response, either related to insulin resistance
or to increased glucagon-like-peptide 1;
(b) renal glycosuria;
(c) defects in glucagon response;
(d) high insulin sensitivity, probably the most frequent cause (50-70%), which is not adequately compensated by hypoinsulinemia and thus cannot be measured by indices of insulin sensitivity
such as the homeostatic model assessment.
Such situations are frequent in very lean people, or after massive weight reduction, or in women with moderate lower body overweight. PRH is influenced by patients alimentary habits (high carbohydrate-low fat diet, alcohol intake). Thus, diet remains the main treatment, although glucosidase inhibitors and some other drugs may be helpful.
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