Abstract
Although obesity has been viewed traditionally as a disease of excess nutrition, evidence suggests that it may also be a disease of malnutrition. Specifically, thiamin deficiency was found in 15.5–29% of obese patients seeking bariatric surgery. It can present with vague signs and symptoms and is often overlooked in patients without alcohol use disorders. This review explores the relatively new discovery of high rates of thiamin deficiency in certain populations of people with obesity, including the effects of thiamin deficiency and potential underlying mechanisms of deficiency in people with obesity. The 2 observational studies that examined the prevalence in preoperative bariatric surgery patients and gaps in our current knowledge (including the prevalence of thiamin deficiency in the general obese population and whether the current RDA for thiamin meets the metabolic needs of overweight or obese adults) are reviewed. Suggestions for future areas of research are included.
Keywords: bariatric surgery, malnutrition, obesity, thiamin deficiency, diet, reducing, micronutrients, vitamin B deficiency
Introduction
The prevalence of obesity in the United States has more than doubled since 1980, with 35% of American adults being obese in 2012 (1). This is of great consequence because obesity has been associated closely with an increased risk of multiple comorbidities, including type 2 diabetes mellitus, cardiovascular disease, obstructive sleep apnea, metabolic syndrome, and malignancy, as well as increased disease-specific and all-cause mortality (2–4). There is evidence suggesting that obesity has now overtaken smoking as the leading cause of preventable death in the United States (5), and the health care costs attributable to obesity likely range from $860 to $956 billion, or 15.6–17.6% of total health care costs in this country (6). It is clear that obesity has emerged as 1 of the most important public health threats of the 21st century.
Although obesity has been associated clearly with much comorbidity, malnutrition has not generally been considered 1 of the associated disorders. Rather, obesity has been viewed traditionally as a disease of “over-nutrition” because it often results from excessive caloric intake. However, many obese Americans eat diets that consist of high-calorie, low nutrient-dense processed foods high in fats and simple sugars—foods that are energy dense and contribute to weight gain but are devoid of essential vitamins and minerals. In the past decade, it became more apparent that, despite its overfed state, obesity may actually be a disease of malnutrition. The National Research Council reported that >80% of Americans eat a diet that is below the RDA for vitamins and minerals (7), and the NHANES III survey, which included a cross-sectional nationally representative sample of adults older than 19 y and included 3831 obese subjects, found that deficiencies of multiple nutrients are more common in people with BMIs in the obese range than in normal-weight participants (8). Various possible mechanisms outlined by Kimmons et al. (8) include decreased absorption, increased excretion, varying storage/distribution (e.g., fat sequestering or tissue dispersion), differing metabolism (e.g., catabolic losses, possibly due to increased oxidative stress in obese patients), increased physiologic requirements, or lower absolute total dietary intake; however, there are very few studies available to date to confirm any of these mechanisms.
Thiamin Deficiency
Thiamin (or vitamin B-1) is an essential micronutrient that catalyzes several key biochemical reactions involved in the metabolism of glucose (Figure 1) and is thus critical for normal tissue and organ function. In the Krebs cycle, which occurs within mitochondria, it is an important cofactor for the production of the primary source of energy for cells (ATP); it is also critical in the pentose phosphate pathway, which is a major route for the synthesis of certain neurotransmitters, nucleic acids, lipids, amino acids, steroids, and glutathione. Thiamin is found in lean pork, beef, wheat germ and whole grains, organ meats, eggs, fish, legumes, and nuts. It is not present in fats/oils, polished rice, or simple sugars, nor are dairy products or some fruits and vegetables a good source (Table 1); therefore, it may be difficult for some adults to meet the RDA for thiamin of 1.1 mg/d in women and 1.2 mg/d in men (9). Thiamin concentrations are measured either by direct measurement via HPLC in plasma, whole blood, erythrocytes, or by determination of the activity of a thiamin-dependent enzyme in erythrocytes called transketolase (Figure 1). Erythrocytes lack mitochondria, so they use the pentose phosphate pathway to generate NAD(P)H. Transketolase is a thiamin-requiring enzyme used to catalyze reactions in the pentose phosphate pathway, so an increase in transketolase activity after the addition of thiamin can identify cells deficient in thiamin at baseline. Both direct measurement via HPLC and the erythrocyte transketolase activation assay are precise and yield similar results (10). Because thiamin is water soluble and there are no substantial thiamin stores in the body, people on thiamin-deficient diets or with malabsorption can deplete their reserves within just 2–3 wk, and it is widely known that alcohol abusers are often deficient in thiamin. However, because most modern physicians believe that the Western diet (with its vitamin-fortified food products) precludes overt clinical micronutrient deficiencies, thiamin deficiency is not usually considered in the differential diagnosis of presenting complaints in non-alcoholic patients in the United States (11).
FIGURE 1.
Major biochemical reactions requiring thiamin as a cofactor.
TABLE 1.
Thiamin content of foods and their contribution to the RDA of thiamin for healthy adults (9)
RDA, % |
||||
Food | Serving size | Thiamin, mg | Women | Men |
Rice (white, long-grain, regular, cooked, unenriched) | 0.5 cup (118 mL) | 0.016 | 1.5 | 1.3 |
Snacks (potato chips, plain, salted) | 1 oz (28 g) | 0.018 | 1.6 | 1.5 |
Carrots (baby, raw) | 3 oz (85 g) | 0.026 | 2.4 | 2.2 |
Ice cream (vanilla) | 0.5 cup (118 mL) | 0.027 | 2.5 | 2.3 |
Apples (raw, with skin) | 1 medium | 0.031 | 2.8 | 2.6 |
Strawberries (raw, whole) | 1 cup (237 mL) | 0.035 | 3.2 | 2.9 |
Tortilla chips (yellow, plain, salted) | 1 oz (28 g) | 0.037 | 3.4 | 3.1 |
Beans (snap, green, cooked, boiled, drained) | 0.5 cup (118 mL) | 0.046 | 4.2 | 3.8 |
Candies (milk chocolate bar) | 1.55 oz (44 g) | 0.049 | 4.5 | 4.1 |
Beef (rib eye filet, boneless, trimmed of fat, grilled) | 3 oz (85 g) | 0.049 | 4.5 | 4.1 |
Nuts (almonds) | 1 oz (28 g) | 0.057 | 5.2 | 4.8 |
Chicken (broilers or fryers, meat only, roasted) | 3 oz (85 g) | 0.058 | 5.3 | 4.8 |
Fast foods (sundae, hot fudge) | 1 item | 0.063 | 5.7 | 5.3 |
Yogurt (fruit variety, nonfat) | 6 oz (170 g) | 0.068 | 6.2 | 5.7 |
Fast foods (brownie) | 2 inches (5.1 cm) square | 0.072 | 6.5 | 6.0 |
Rice (brown, long-grain, cooked) | 0.5 cup (118 mL) | 0.094 | 8.5 | 7.8 |
Beans (baked, canned, plain, or vegetarian) | 0.5 cup (118 mL) | 0.12 | 11.1 | 10.2 |
Fast foods (biscuit, with egg and bacon) | 1 item | 0.14 | 12.3 | 11.3 |
Lentils (mature seeds, cooked, boiled) | 0.5 cup (118 mL) | 0.17 | 15.2 | 13.9 |
Fast food (pizza chain, 14-inch pepperoni pizza, thin crust) | 1 slice | 0.18 | 16.2 | 14.8 |
Peas (green, cooked, boiled, drained) | 0.5 cup (118 mL) | 0.21 | 18.8 | 17.3 |
Shake (fast food, chocolate) | 16 oz (473 mL) | 0.22 | 19.8 | 18.2 |
Fast foods (potato, French fried in vegetable oil) | 1 large | 0.26 | 23.8 | 21.8 |
Wheat germ (crude) | 2 tbsp (30 mL) | 0.27 | 24.4 | 22.3 |
Fish (salmon, Atlantic, farmed, cooked, dry heat) | 3 oz (85 g) | 0.29 | 26.3 | 24.1 |
Cereals (instant oatmeal organic, regular) | 1 packet | 0.30 | 27.2 | 24.9 |
Cereals (corn grits, instant, plain, prepared) | 1 cup (237 mL) | 0.31 | 28.5 | 26.1 |
Pork (fresh, loin, tenderloin, lean only, broiled) | 3 oz (85 g) | 0.84 | 76.4 | 70.0 |
Cereals (ready-to-eat, wheat germ, toasted, plain) | 1 cup (237 mL) | 1.9 | 172 | 157 |
Cereals (ready-to-eat, enriched bran flakes) | 1 cup (237 mL) | 2.0 | 180 | 165 |
Because thiamin is an important cofactor in glucose metabolism, its deficiency can lead to severe (or even fatal) cardiovascular and neurologic complications, including heart failure, neuropathy leading to ataxia and paralysis, confusion, or delirium. Generally, cardiac effects are referred to as wet beriberi, the peripheral neurologic manifestations are called dry beriberi, and delirium or mental confusion are termed Wernicke’s encephalopathy. Although the full-blown classical deficiency syndromes of beriberi or Wernicke’s encephalopathy occur relatively rarely in the United States and only in patients with severe thiamin deficiency, marginal deficiency (in which thiamin stores are sufficiently depleted to affect a patient’s well-being and to be detected on laboratory tests but not depleted enough to create the classical clinical signs) may give rise to symptoms that are more vague and often overlooked (Table 2). Demonstrating this point, in 1943, a group of researchers published a series of small experiments performed on young healthy women in which they observed their clinical outcomes after extended periods of intentional dietary thiamin depletion (12). The investigators compared the women with controls who were not deprived of thiamin and found that they developed a myriad of vague signs and symptoms, including mental fatigue and emotional lability, paresthesias, generalized weakness, myalgias and back pain, nausea and vomiting, and decreased ability to perform physical activity or work. These somatic complaints were reversed after their thiamin amounts were repleted (12). Although these experiments have obvious limitations (they were only done on a very small number of volunteers who were not randomly assigned or unaware of the treatment and so, by today’s standard, could be considered unethical), the findings are compelling nonetheless. It is plausible that states of moderate thiamin deficiency would go undiagnosed because the signs and symptoms are vague and common to many different disorders. Indeed, a small observational study of 36 elderly hospitalized community-dwelling patients without known nutritional deficiencies found that 31% had marginal thiamin deficiency (defined by the authors as a 15–24% increase in erythrocyte transketolase activity after the addition of thiamin pyrophosphate, with normal being <15%), and 17% of patients had definite thiamin deficiency (defined as >25% increase in erythrocyte transketolase activity after the addition of thiamin pyrophosphate). Delirium occurred in 76% of thiamin-deficient patients, but was only present in 32% of patients with normal thiamin status (P < 0.025) (13). This lends credence to the idea that clinically relevant thiamin deficiency may be quite common but that the diagnosis is overlooked because of the ambiguity of signs and symptoms; the prevalence of thiamin deficiency in the general US population is not known.
TABLE 2.
Signs and symptoms of thiamin deficiency
Gastrointestinal | Neurologic | Cardiovascular |
Anorexia | Irritability, emotional lability | Chest pain |
Nausea and vomiting | Depression | Tachycardia |
Dysphagia | Fatigue | Cardiomegaly |
Abdominal discomfort | Generalized weakness | Decompensated systolic heart failure (peripheral/pulmonary edema) |
Constipation | Sleep disturbance | Widened pulse pressure |
Myalgias | Hypotension | |
Muscle cramps | Cardiogenic shock | |
Peripheral neuropathy (including paresthesias, neuropathic pain, decreased reflexes, and decreased vibratory/position) | ||
Sense | ||
Ataxia | ||
Ophthalmoplegia | ||
Nystagmus | ||
Blindness | ||
Confusion | ||
Agitation | ||
Memory loss | ||
Coma |
There are several different ways that individuals might become deficient in thiamin (Table 3), including decreased oral intake and/or absorption from the diet, increased losses, or increased depletion through metabolism. Although thiamin is abundant in certain foods, such as whole grains and legumes, diets that primarily consist of simple sugars, fats, or excessive alcohol are low in the vitamin. Furthermore, substantial losses of thiamin occur during cooking or other heat processing, and polyphenolic compounds in coffee and tea can inactivate thiamin. Similarly, raw fish and shellfish (and some human gut flora) contain thiaminases that also destroy thiamin (11, 14). Diuretics, such as furosemide, increase the loss of thiamin in the urine, and peritoneal and hemodialysis removes thiamin from the circulation as well (11, 14). Studies showed a dramatic increase in urinary thiamin excretion in patients with diabetes compared with normal volunteers (24-fold in patients with type 1 diabetes and 16-fold with type 2 diabetes) (15). Increased thiamin requirements result from certain conditions, including hypermetabolic states, strenuous activity, acute illness or fever, pregnancy and lactation, adolescent growth, major trauma, and major surgery (11, 16). Thiamin is absorbed primarily in the duodenum mainly through active transport, so individuals who have undergone bariatric surgery to treat severe obesity (especially surgical procedures that bypass the duodenum, such as the Roux-en-Y gastric bypass) are particularly at risk of developing thiamin deficiency after surgery because of a combination of factors: the surgical stress leading to increased thiamin demand, malabsorption of the vitamin in the gastrointestinal tract due to bypass of the duodenum, and the significantly decreased oral intake (sometimes exacerbated by nausea and vomiting) that occurs after surgery as a result of restriction of the stomach size. Indeed, many case reports and observational studies documented the occurrence of Wernicke’s encephalopathy after bariatric surgery even in non-alcoholic individuals (17–23), and the identification of thiamin deficiency as a potential postoperative complication led to the recommendations that all patients be screened for thiamin deficiency before bariatric surgery and that all bariatric surgery patients receive thiamin supplementation after surgery (24).
TABLE 3.
Potential mechanisms of thiamin deficiency
Decreased intake/absorption | Increased destruction/inactivation | Excessive losses | Increased use/metabolism |
Poor diet quality | Polyphenols (e.g., in coffee, tea, and betel nut) | Diuretics | High-carbohydrate diets |
Excessive alcohol | Thiaminases (e.g., in raw seafood and human gut flora) | Peritoneal or hemodialysis | Hypermetabolic states (e.g., hyperthyroidism) |
Excessive simple sugars, milk products, fats | Hypomagnesemia | Renal losses in diabetes | Strenuous activity |
Heat processing of food | Acute illness/fever | ||
Irradiation of food | Pregnancy and lactation | ||
Inadequate whole grains/legumes | Prolonged contact with amino acids in parenteral nutrition | Adolescent growth | |
Major trauma | |||
Anorexia | Major surgery | ||
Prolonged emesis | Refeeding syndrome | ||
Intestinal malabsorption (e.g., duodenal bypass, short gut syndrome, Crohn’s disease, proton pump inhibitors) | Chemotherapeutic agents (e.g., 5-flourouracil) |
Although the mechanisms underlying thiamin deficiency in bariatric surgery patients postoperatively are clear, a surprising finding is that many obese patients are found to be deficient in thiamin before undergoing surgery. In fact, the prevalence of thiamin deficiency in preoperative bariatric surgery patients has been reported to be between 15.5% (16) and 29% (25), with Flancbaum et al. (25) finding a significantly higher prevalence of thiamin deficiency in African Americans (31%) and Hispanics (47.2%) than in Caucasians (6.8%). The reasons for racial differences are unclear. To our knowledge, these 2 retrospective studies are the only ones that examined the prevalence of thiamin deficiency in the obese; they were relatively small, with 303 subjects and 379 subjects, respectively, but the findings were notable nonetheless. Although there are clear theoretical mechanisms for the development of postoperative thiamin deficiency, most of these etiologies should not be present in obese patients preoperatively. Therefore, other reasons for thiamin deficiency in this population must be sought.
There is speculation that the primary etiology for thiamin deficiency in people with obesity is a diet high in simple sugars and low in whole grains, legumes, and other whole foods that naturally contain thiamin. Not only do simple sugars lack thiamin, but the metabolism of foods high in sugar requires relatively high amounts of thiamin and may therefore accelerate its depletion (11, 16, 26). Indeed, this concept is supported by a small study in 12 healthy volunteers that found that an increase in dietary carbohydrate (from 55% to 65% to 75% of total energy intake for 8 d) although thiamin intake, total energy intake, and physical activity levels remained constant caused a decrease of plasma and urine thiamin amounts (27). Although the effect of increasing carbohydrate intake on thiamin amounts was not tested similarly in obese subjects, it is reasonable to assume that they will have the same increased thiamin requirements and in fact may have substantially higher thiamin needs because of their higher absolute energy and carbohydrate intake.
Although the effect of increased carbohydrate intake was not evaluated specifically, several studies examined the effect of intentional weight loss (due to changes in diet) on micronutrient amounts in overweight and obese subjects. One study followed 32 obese subjects who were maintained exclusively on a very low-calorie formula diet for 12 wk; the protein-rich formula (Optifast 800 formula; Nestlé) consisted of 800 kcal/d (50% from carbohydrate) and included all vitamins, minerals, and trace elements in amounts to meet the RDAs for healthy adults. Although thiamin amounts were not tested specifically after the weight-loss intervention, several other micronutrients were tested; the investigators found that pre-existing deficiencies of vitamin C, zinc, iron, and selenium either worsened or could not be corrected by the diet containing micronutrient amounts meeting the RDAs (28), and they concluded that micronutrient deficiencies in obesity may not only be caused by diets that fail to meet the RDA but rather that the RDAs of micronutrients may be inadequate to meet the metabolic demands for some micronutrients in obese people.
A subsequent randomized controlled trial compared the effects of a high-protein, high-thiamin weight-loss diet (consisting of 43% carbohydrate, 33% protein, 22% fat, and 2.8 mg/d thiamin, more than double the RDA for thiamin) with a high-carbohydrate, adequate-thiamin diet (consisting of 53% carbohydrate, 19% protein, 26% fat, and 1.1 mg/d thiamin, meeting the RDA for thiamin) on the thiamin status of 100 overweight or obese subjects with type 2 diabetes mellitus. Although baseline thiamin amounts were collected, unfortunately, neither energy intake nor thiamin intake was assessed at baseline. After 16 wk, all subjects lost similar amounts of weight (∼11 kg); subjects in the high-thiamin group had no change in erythrocyte thiamin amounts from baseline, whereas subjects in the adequate-thiamin group demonstrated a significant decrease in erythrocyte thiamin amounts (29). The investigators concluded that, even with modest weight loss (less than the usual range seen after bariatric surgery), cellular thiamin amounts decreased even when the diet consumed met the RDA for thiamin intake.
Although most studies do not report on baseline thiamin consumption in overweight and obese people, 1 small study conducted in Spain did evaluate the thiamin intake of subjects at baseline and after a dietary intervention (30). Fifty-seven young women with BMIs of 24–35 kg/m2 were randomly assigned to follow 1 of 2 diets: 1) a hypocaloric diet with increased intake of fortified breakfast cereals; or 2) a hypocaloric diet with increased intake of vegetables. The mean BMI at baseline was ∼28 kg/m2, putting most of the subjects in the overweight (rather than obese) range; baseline energy intake was collected via 3-d food records. Thiamin intake was calculated to be ∼2 mg/d at baseline, which was double the RDA; serum thiamin amounts were also adequate at baseline. However, after 6 wk of following the assigned diets, subjects in the cereal group significantly increased their thiamin intake and serum thiamin amounts, whereas subjects in the vegetable group significantly decreased daily thiamin consumption (to amounts below the RDA) and also developed decreased serum thiamin amounts. Limitations of this study include its relatively small size, short duration, and limited external validity in that subjects were mostly overweight rather than obese; however, one might infer from these results that thiamin intake and serum status are normal in overweight (and possibly obese) people in energy balance but that energy-restricted weight-loss diets (often higher in thiamin-poor vegetables) may lead to decreased thiamin intake and induce thiamin deficiency for many people.
Gaps in the Literature and Directions for Future Research
Dietary thiamin needs are expressed generally as either a total amount per day in milligrams or a percentage of total energy intake. However, little is known about whether thiamin requirements vary based on the amount of carbohydrate eaten; similarly, to our knowledge, there are no published studies to date that determined thiamin requirements in overweight and obese adults. Both of the prospective trials discussed above (28, 29) suggest that the RDAs for micronutrients may not be adequate for obese people who are engaged in weight-loss efforts; however, to date, to our knowledge, there are no studies that examined whether the metabolic changes and stress that occur during active weight loss increase the body’s demands for certain micronutrients (including thiamin) or whether the current RDAs are simply inadequate for obese people in general. Very few studies to date examined the thiamin status of free-living obese individuals at baseline who are not engaged in weight-loss efforts. In fact, the prevalence of thiamin deficiency of 15.5–29% reported in preoperative bariatric surgery patients (16, 25) may not reflect the general obese population, because all patients qualifying for bariatric surgery must have actively engaged in behavioral weight-loss efforts (including dieting) for a minimum of 3–6 mo before surgery to qualify for surgery. As Ortega et al. (30) found in 2009, energy-restricted diets may lead to thiamin deficiency in overweight people who were not deficient at baseline. Therefore, the prevalence of thiamin deficiency in the preoperative bariatric surgery population may not accurately reflect the prevalence of thiamin deficiency in the general (non-dieting) obese population. Furthermore, many obese bariatric surgery candidates also have comorbid diabetes, which confounds the issue further given that the prevalence of thiamin deficiency in patients with diabetes has been reported to be anywhere from 17% to 79% (15, 31–34).
Current RDAs for micronutrients apply to normal, healthy adults but may not meet the metabolic needs of overweight or obese adults regardless of their intake of simple sugars or engagement in caloric restriction or other weight-loss efforts. Alternatively, the presence of diabetes may be confounding the micronutrient status of obese adults. Future research should address these gaps in our knowledge, because understanding the impact of obesity on micronutrient status is an important public health issue. First, researchers should determine the prevalence of thiamin deficiency in the general population of people with overweight and obesity, controlling for potentially confounding factors, such as recent dieting, use of vitamin supplements, the presence of diabetes, and the use of diuretics. If a high prevalence of thiamin deficiency is found in non-dieting overweight and/or obese people, additional studies to elucidate the underlying mechanisms will be warranted, and recommendations for a change in the RDA for thiamin (and possibly for other micronutrients) may be indicated. Additionally, screening recommendations for thiamin deficiency in obese patients may be appropriate if future research confirms a high prevalence of thiamin deficiency in non-dieting obese patients. Alternatively, if thiamin amounts are normal in the general population of people with obesity, then it is likely that the RDA for thiamin is adequate for obese adults but not for those engaging in weight-loss efforts. In that case, additional studies to determine the optimal dose of thiamin required during weight-loss efforts would be valuable. Specifically, thiamin requirements might differ for diets with varying macronutrient compositions, so prospective studies that evaluate changes in thiamin amounts in patients on diets with variable carbohydrate intake would be worthwhile, and recommendations for the routine use of micronutrient supplementation (including thiamin) during periods of caloric restriction may be needed. Furthermore, vigorous exercise might also increase thiamin demand in patients engaging in weight-loss efforts, so studies designed to evaluate changes in thiamin amounts based on exercise dose would also be warranted. For now, it would behoove clinicians to consider the diagnosis of thiamin deficiency in obese or dieting patients with vague signs and symptoms, such as gastrointestinal symptoms, mood or sleep disturbances, paresthesias, or heart failure, that have not otherwise been explained.
Acknowledgments
Dr. Jean Gutierrez provided general support and reviewed the first draft. JCK conceived of this review and performed the literature search. All authors have read and approved the final manuscript.
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