30-04-2022 Brunch was finally tabled towards 1600hrs for which I risked sifting the hot beans as the gay-husband had left. No supper. If they kill me before 10m+ damages pay, my WILL's as on email signatures. SOS. { https://wp.me/pb6oyO-6k5 [ As Uhuru's GoK compromises my latest 7-8 page statement charges of OB61/23/08/2021 ( https://wp.me/pb6oyO-63J ) on SOA No. 3 of 2006 and PADVA of 2015, even as they brood-sit pretty on my now 9yrs 10-months 10m+ damages ( https://wp.me/pb6oyO-65w ), imposing a pauperism-bachelorhood on me at 44yrs compromising my dating and marriage, I routinely need bare-minimums to meet hygiene-and-decency basics including now: a Bic-razor, a belt, and a wardrobe. Ain't living or working in narcissistic-Godzilla-Raila's Luo-Nyanza. SOS. #FreedBritney #turpinfamily Otherwise, finally found the problem with my digesting carbohydrates / starch intolerances as demonstrated below, though I've only perused and I'm yet to get fully acquainted with the details. The reason I've been avoiding the witches'-nest un-thrashed -maize and beans aka 'Nyoyo' in Luo and boiled tubers which if are roasted takes away all the intolerance and I can eat and digest a pile..... what got the jealousy-witches' eyes popping-out after which they never roasted the tubers again selecting to adopt their cyclic-ritual peristalsis-triggering diets as noted in the title above { routine customary hunger-torture, stomach-constricting, muscular-dystrophy exploiting-starvations as Uhuru's 'Zombie-Child Physique' making-of-archetypes prehistoric-descendant-culture Death-Cult's imposed penniless-pauperism renders me largely indoors for want of stipends }. SOS. The links within links detailing the same can be found here too : ( https://wp.me/pcMu0M-G ).
The quickie-prostitute and gay-husband psychic-cannibal-vampire-witches ( substantiated technical descriptive terms ) are dying of jealousy with improvised-gym body-building exercises therapy I'd begun to stay a week+ without going for a big calls like I used during my college days when I was such a dude / block with proper gym going close to two weeks without shitting! They make sure un-thrashed-maize and beans are cooked every two to three or four days to align with their zombie-death-occult.I pray your divine interventions to fast-track my 9yrs 10-months compensatory and punitive damages adding to backlog statistics now with the Ombudsman / CAJ / OJO. Thank you in advance, Yours Faithfully, Erick Mango.Carbohydrate Intolerance - Gastrointestinal Disorders - MSD Manual Professional Edition (msdmanuals.com)
Carbohydrate Intolerance
By
Atenodoro R. Ruiz, Jr.
, MD, The Medical City, Pasig City, Philippines
Last full review/revision Feb 2021| Content last modified Feb 2021
CLICK HERE FOR PATIENT EDUCATION
Carbohydrate intolerance is the inability to digest certain carbohydrates due to a lack of one or more intestinal enzymes. Symptoms include diarrhea, abdominal distention, and flatulence. Diagnosis is clinical and by a hydrogen breath test. Treatment is removal of the causative disaccharide from the diet.
Carbohydrate intolerance is a malabsorption syndrome.
Pathophysiology of Carbohydrate Intolerance
Disaccharides are normally split into monosaccharides by disaccharidases (eg, lactase, maltase, isomaltase, sucrase [invertase]) located in the brush border of small-bowel enterocytes. Undigested disaccharides cause an osmotic load that attracts water and electrolytes into the bowel, causing watery diarrhea. Bacterial fermentation of carbohydrates in the colon produces gases (hydrogen, carbon dioxide, and methane), resulting in excessive flatus, bloating and distention, and abdominal pain.
Overview of Lactose Intolerance
VIDEO
Etiology of Carbohydrate Intolerance
Enzyme deficiencies can be
- Congenital (eg, rare deficiencies of lactase or sucrase-isomaltase)
- Acquired (primary)
- Secondary
Acquired lactase deficiency (primary adult hypolactasia) is the most common form of carbohydrate intolerance. Lactase levels are high in neonates, permitting digestion of milk; in most ethnic groups (80% of blacks and Hispanics, > 90% of Asians), the levels decrease in the post-weaning period rendering older children and adults unable to digest significant amounts of lactose. However, 80 to 85% of whites of Northwest European descent produce lactase throughout life and are thus able to digest milk and milk products. It is unclear why the normal state of > 75% of the world's population should be labeled a "deficiency."
Secondary lactase deficiency occurs in conditions that damage the small-bowel mucosa (eg, celiac disease, tropical sprue, acute intestinal infections [see Gastroenteritis]). In infants, temporary secondary disaccharidase deficiency may complicate enteric infections or abdominal surgery. Recovery from the underlying disease is followed by an increase in activity of the enzyme.
Symptoms and Signs of Carbohydrate Intolerance
Symptoms and signs of carbohydrate intolerance are similar in all disaccharidase deficiencies. A child who cannot tolerate lactose develops diarrhea after ingesting significant amounts of milk and may not gain weight. An affected adult may have watery diarrhea, bloating, excessive flatus, nausea, borborygmi, and abdominal cramps after ingesting lactose. The patient often recognizes early in life that dairy causes gastrointestinal problems and avoids eating dairy products. Symptoms typically require ingestion of more than the equivalent of 250 to 375 mL (8 to 12 oz) of milk. Diarrhea may be severe enough to purge other nutrients before they can be absorbed. Symptoms may be similar to and can be confused with irritable bowel syndrome.
Pearls & Pitfalls
- Most people with lactase deficiency can tolerate up to 250 to 375 mL (8 to 12 oz) of milk; symptoms that occur after consuming much smaller amounts may suggest another diagnosis.
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Diagnosis of Carbohydrate Intolerance
- Clinical diagnosis
- Hydrogen breath test for confirmation
Lactose intolerance can usually be diagnosed with a careful history supported by dietary challenge. Patients usually have a history of diarrhea and/or gas after ingestion of milk and dairy foods; other symptoms, such as rash, wheezing, or other anaphylactic symptoms (particularly in infants and children), suggest a cow's milk allergy. Milk allergy is rare in adults and also may cause vomiting and symptoms of esophageal reflux, which are not manifestations of carbohydrate intolerance. The diagnosis of lactose intolerance is also suggested if the stool from chronic or intermittent diarrhea is acidic (pH < 6) and can be confirmed by a hydrogen breath test or a lactose tolerance test that indicates malabsorption. These test results should be correlated with symptoms for assessment of lactose intolerance; a few standardized questionnaires are currently being validated.
In the hydrogen breath test, 50 g of lactose is given orally and the hydrogen produced by bacterial metabolism of undigested lactose is measured with a breath meter at 2, 3, and 4 hours postingestion. Most affected patients have an increase in expired hydrogen of > 20 parts per million over baseline. Sensitivity is 78% and specificity is > 95% (1).
The lactose tolerance test is less sensitive, about 75%, although specificity is > 95%. Oral lactose (1.0 to 1.5 g/kg body weight) is given. Serum glucose is measured before ingestion and 60 and 120 minutes after. Lactose-intolerant patients develop diarrhea, abdominal bloating, and discomfort within 20 to 30 minutes, and their serum glucose levels do not rise to > 20 mg/dL (< 1.1 mmol/L) above baseline.
Diagnosis reference
- 1. Gasbarrini A, Corazza GR, Gasbarrini G, et al: Methodology and indications of H2-breath testing in gastrointestinal diseases: The Rome Consensus Conference. Aliment Pharmacol Ther 29 (supplement 1):1–49, 2009. doi: 10.1111/j.1365-2036.2009.03951.x
Treatment of Carbohydrate Intolerance
Carbohydrate malabsorption is readily controlled by avoiding dietary sugars that cannot be absorbed (ie, following a lactose-free diet in cases of lactase deficiency). However, because the degree of lactose malabsorption varies greatly, many patients can ingest up to 375 mL (18 g of lactose) of milk daily without symptoms. Yogurt is usually tolerated because it contains an appreciable amount of lactase produced by intrinsic Lactobacilli. Cheese contains lower amounts of lactose than milk and is often tolerated, depending on the amount ingested.
For symptomatic patients wishing to drink milk, lactose in milk can be predigested by the addition of a commercially prepared lactase, and pretreated milk is now available. Enzyme supplements should be an adjunct to, not a substitute for, dietary restriction. Lactose-intolerant patients must take calcium supplements (1200 to 1500 mg/day).
Key Points
- Disaccharide deficiency (usually of lactase) can be acquired or, rarely, congenital.
- Undigested disaccharides, such as lactose, create an osmotic load that causes diarrhea.
- Intestinal bacteria metabolize some undigested disaccharides, producing gases that cause distention and flatus.
- Assess carbohydrate intolerance clinically and confirm diagnosis by doing a hydrogen breath test.
- Dietary restriction is usually adequate treatment.
Starch intolerance - Food Intolerance (Food Intolerance Diagnostics) (foodintolerances.org)
Starch intolerance
Sucrose, maltose and starch intolerance
Causes
Individuals with congenital sucrase-isomaltase enzyme deficiency (CSID or GSID) have reduced digestion of the sugars sucrose (table sugar) and maltose (found in grains) and sometimes also of starch in the small intestine.
The deficiency may affect several enzymes (sucrose, maltase, isomaltase and lactase), is caused by multiple possible genetic mutations and is therefore present from birth onwards. Depending on the mutation, sucrose, maltose, starch and sometimes also lactose digestion are impaired, leading to varying degrees of intolerance of these carbohydrates. The intolerance symptoms are caused by a reduced breakdown in the small intestine and subsequent fermentation by the flora (microbiome) in the lower intestine.
Inheritance is by an autosomal recessive pattern, i.e. both parents must have the mutation for the child to develop the full-blown disease. The parents (heterozygotes) typically show no or only minor signs and symptoms of the condition...
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