study finds Vitamin D levels elevated in FORL and cat food

Issues involving dental care. Questions, answers, theories, and evidence.
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study finds Vitamin D levels elevated in FORL and cat food

Postby malernee » Wed Mar 24, 2004 7:56 am

DENTAL NECK LESIONS IN CATS
(Odontoclastic Resorptive Lesions)

General Information
Feline dental neck lesions are a dental disorder in which portions of the teeth dissolve or are resorbed at the gum line. It is caused by inflammation of the lining (periodontium) of the socket that surrounds and houses the root of the tooth. It may be severe enough to destroy the exposed portion (crown) of the tooth, leaving only the tooth roots. In such cases, the sensitive internal structures of the tooth remain exposed, and the cat experiences considerable pain and discomfort.
Signs can include refusal to eat, loss of weight, chattering of the teeth, drooling, and depression. It has been estimated that 20% to 60% of all cats are affected, with 2 to 5 teeth involved in individual cats. It is possible for cats to experience this disorder without the gums showing any outward signs. Generally, however, the gum line is reddened, swollen, and tender. The premolars and molars are most often affected, followed by the canines (fangs) and smaller front teeth (incisors).
Removing tartar accumulations by regular dental hygiene at home and periodic, professional dental cleaning plays a very important role in preventing the disease.
Important Points in Treatment
1. Radiographs (x-rays) are generally required to determine the extent of damage to the teeth. If blood tests have not been recently performed, they may be required, especially for individuals over 8 years of age. A cat of any age may require blood studies to assess general health before undergoing general anesthesia or to make certain other underlying disorders do not exist.
2. Treatment includes dental restoration procedures or extraction of the diseased teeth. The severity of the condition, the age and general health of the animal, availability of specialized treatment, and economic considerations dictate the method of treatment.
3. Tooth extraction is the most common treatment, but your veterinarian will discuss the different choices with you.
4. Other recommendations/comments:




Could my Cat have a FORL?
According to information presented at the American Veterinary Dental Forum, if your cat is over five years old, there is a 72% chance he or she has a painful feline odontoclastic resorptive lesion (FORL). These dental resorptions once called cat cavities or neck lesions can occur in any tooth. The most commonly affected teeth are the lower premolars.

Unlike cavities in humans, which are the result of bacterial enzymes and acids digesting the teeth, the cause of FORLs are unknown. Specifically, cells known as odontoclasts are found in the defects causing the tooth structure to dissolve. What triggers this reaction has not been determined for certain but a reaction to plaque on the teeth seems to be the major factor.

Cats affected with FORLs may show hypersalivation, oral bleeding, or have difficulty chewing. A majority of affected cats do not show obvious signs but are in pain. A cotton tipped applicator applied to the suspected FORL causes pain with jaw spasms when the FORL is touched.

The FORL can present in many stages -- initially (Stage I) an enamel defect is noted. The lesion is usually minimally sensitive in because it has not entered the dentin. Therapy of this defect usually involves thorough cleaning, polishing, and smoothing the defect with a dental drill.


Class 2 FORL
In Stage 2, lesions penetrate the enamel and dentin. These teeth may be treated with glass ionomer restoratives, which release fluoride ions to desensitize the exposed dentin, strengthen the enamel, and chemically bind to tooth surfaces. The long term (greater than two years) effectiveness of restoration of Stage 2 lesions have not been proven.




Grade 3 FORL
X-rays are essential to determine if the lesions have entered the pulp chamber (Stage 3) requiring either root canal therapy or extraction. Here the lesion it is not only painful, but bacteria in the mouth now have easy access to the tip of the tooth root where an abscess can develop. Tooth root abscesses have been well documented as chronic sources of infection that can lead to infections on the heart valves, in the liver, kidneys, spleen, joints, bones and central nervous system.


Stage 4 FORL
In Stage 4 FORL, the crown has been eroded or fractured. Gum tissue grows over the root fragments leaving a sometimes painful bleeding lesion upon probing. Treatment requires extraction of the root fragments if they appear inflamed or painful to the patient.

At least monthly examine your cat’s mouth for FORLs. Take a Q-tip and gently place it against the area where the tooth meets the gum. If there is pain or bleeding a trip to the veterinarian is in order. Your best friend will thank you.
***
below information was promoted by a boarded dental vet on a for vet only newsgroup

Dental resorptive lesions in dogs are very interesting, just as they are in cats, humans, pigs, etc etc. Etiology for any of them has yet to be proven. The current most popular theory in humans is "abfraction" from mild malocclusive forces directed to the cervical area of the teeth or the roots. My favorite theories for the cat lesions are that there are 2 different types with separate etiologies: one from abfraction, and the other from periodontitis (this is theory only - not shown).

The dog resorptions often show very little periodontal disease, no pockets etc. Sometimes they appear as a "pink spot" on the crown of an otherwise normal-appearing tooth, caused by internal resorption that started on the root.

I have not seen an association with endocrine or other systemic disease
******
new theory about what causes FORL

Dentistry - FORL
FORL is the abbreviation for Feline Odontoclastic Resorptive Lesions, which are very painful erosions in the roots/crowns of cat teeth. This condition was almost unheard of before 1960. Since their occurrence was noted numerous hypothesis as to the cause have been made, but none of these have proved to be correct.

In November 2003 the American Veterinary Dental Society hosted their annual dental forum at which a paper was presented which identified a cause - cat's that develop this condition have marked elevations in Vitamin D levels in their blood. So why is this occurring?

Unlike humans and herbivores, dogs and cats are not able to synthesize vit D3 and depend on dietary intake. When vit D3 contents of commercial cat foods were evaluated, 20 of 49 canned cat foods had excess of 30 times the vit D3 requirement and 15 were in excess of a maximal level of 10,000 IU/kg diet dry matter (recommended is 500 IU/Kg). It has also been found that administration of excess vit D resulted in dental and periodontal conditions that resembled radiographic and histopath FORL lesions. So it appears that finally there may be a break through in the cause of FORLs. Lets hope the pet food companies take this information seriously and act to remedy those products with too high a level.

Another item from this conference is that the use of Fosamax (a drug used for treating osteoporosis in people during menopause) has been shown to reduce the progression of this disease if caught early enough and in addition prevents further lesions developing. We are currently looking into the use of this drug in more detail, if it lives up to early expectations we will start prescribing it for appropriate cases.
********
Notes
Risk Factors for Odontoclastic Resorptive Lesions in Cats

Janet M. Scarlett, DVM, PhD; John Saidla, DVM; Jennifer Hess, BS
Journal of the American Animal Hospital Association
May 1, 1999



The full text of the article is below. To see the complete article with pictures, graphs, and other figures, you may click here to view the PDF version.
Janet M. Scarlett, DVM, PhD; John Saidla, DVM; Jennifer Hess, BSA cross-sectional study evaluating potential risk factors for odontoclastic resorptive lesions (ORL) in feline teeth was conducted. Owners of 32 cats with ORL and 27 cats without ORL were interviewed regarding their respective cat’s demographic characteristics, diet, and medical and dental histories. Four factors were identified as significantly associated with ORL using unconditional logistic regression. A history of dental disease (gingivitis, calculus, or periodontal disease; odds ratio [OR], 4.5); city residence (OR, 4.4); and being an exclusively indoor cat (OR, 4.5) were associated with an increased risk for ORL. Consumption of commercial treats (OR, 0.3) appeared protective for ORL.

J Am Anim Hosp Assoc 1999;35:188–92.

Introduction

Tooth destruction from odontoclastic resorptive lesions (ORL) results in a painful dental condition of cats. Odontoclasts attack and begin to resorb teeth, either externally or internally.1,2 Externally they attack at the neck or cervical area of the tooth, often extending into the tooth root and surrounding alveolar area. Internally, they attack the tooth through the apical foramen and can subsequently enter into the root and dentin. In the early stages, cats are asymptomatic; but as the disease progresses and dentinal tubules and/or pulp are exposed, the lesions become increasingly sensitive and painful. Cats may present with a history of poor appetite or anorexia, eating on one side of the mouth, weight loss, and depression.3–5 External lesions may be difficult to identify if they remain hidden beneath the gingiva or calculus. As the lesions progress, they are often associated with gingival inflammation, bleeding or hyperplasia, and increasing loss of tooth substance. Ultimately, part or all of the affected teeth are lost. Characterizing the full extent of root and alveolar bone involvement requires dental radiographs.4,6

Odontoclastic resorptive lesions are common, affecting 20% to 67% of cats receiving dental care,7 and the prevalence varies with the characteristics of the population studied. In a recent study of cats undergoing a wide range of procedures requiring anesthesia in a private veterinary practice in Wisconsin, 48% of cats examined had one or more ORL;8 this compares closely with an estimate of 52% for a similar sample in Australia.9 The frequency is probably higher, since many lesions are subgingival and difficult to identify, and missing teeth may have been lost because of ORL.7 Despite the variability in prevalence estimates, the frequency of ORL appears to have increased over time. A recent reexamination of the teeth in 80 cat skulls examined originally by Cloyer in 1936 found one skull (1.3%) with ORL;7 a pre-1950 skull series had a 0.4% prevalence, while a post-1970 skull series had 26.5% of skulls with lesions.10 This apparent increase in the prevalence, however, may reflect changes in the age distribution of the cat populations examined.10

Despite a high prevalence, the cause(s) of ORL is unknown. The lesions were originally confused with caries11 which result from demineralization of the tooth enamel by toxins produced by carbohydrate-fermenting bacteria. Unlike caries, however, ORL occur when activated odontoclasts resorb tooth and bone tissue. In response, bone and cementum tissue initiate remodeling, odontoclastic activity continues, and the process repeats itself until ankylosis (i.e., fixation of the root in the alveolus through destruction of the periodontal ligament and lamina dura) occurs, the tooth is permanently damaged, and the root is fixed into the alveolar bone.12

Odontoclasts are normally active only in young animals in resorption of the roots of deciduous teeth, facilitating loss of these teeth and making room for the permanent dentition. In cats with ORL, these cells are inappropriately stimulated to differentiate and become active for reasons that are not well understood. The apparent increase in the prevalence suggests some change(s) in the environment of cats that influences mechanisms that affect the odontoclasts, and the search for some environmental risk factor(s) important in the etiology of this disease has begun.

Numerous hypotheses regarding the etiology have been proposed; they include chronic regurgitation due to hair balls;10,13 a natural progression of periodontal disease;4,13 associations with stomatitis potentially caused by feline calici, feline leukemia, and feline immunodeficiency virus infections;14 nutritional factors such as acidification of dry cat foods;15 hypervitaminosis A from consumption of raw liver;5,16 nutritional hyperparathyroidism;13 inadequate dietary calcium (e.g., homemade diets);15 other dietary factors (e.g., feeding certain brands of nongrocery cat foods or certain table foods);17 and more recently, low magnesium diets.8

This cross-sectional study was initiated to examine risk factors associated with ORL.

Materials and Methods

All cats presented for dental prophylaxis to the dental section of the Community Practice Service of the Companion Animal Hospital at Cornell University between February and July 1994 were identified. Cats with ORL were eligible for inclusion in the case group, and those without lesions were randomly sampled to serve as controls. Cats were evaluated primarily by Dr. Saidla. Cats were anesthetized for dental prophylaxis. The entire mouth was thoroughly examined for dental pathology, and the data was recorded in the medical record by an experienced examiner. Each tooth was probed with a color-coded probe, looking for subgingival lesions, gingival recession, extrusion of teeth, very small enamel lesions or pits, loss of tooth crowns with retained roots, and hyperplasia of the gingiva into enamel defects. The degrees of gingivitis and periodontal disease were also noted. The following data was retrieved from each cat’s medical record: the date of diagnosis of ORL; history of dental disease; the number and location of lesions in the mouth; prior extractions; types of other oral pathology; prescriptions for antibiotics and other medications; and disease diagnoses prior to the diagnosis of ORL.

Owners of both case group cats and control cats were asked to participate in a 15- to 20-minute telephone interview during which they were asked to describe their cat’s demographic characteristics (e.g., age, sex), diet (e.g., type of food, frequency of feeding, table food), number of cats owned, time spent outdoors, previous use of medications, and medical history at and prior to the date of diagnosis of ORL. All owners were told the study was an assessment of factors affecting oral health. Interviewers were blind to whether clients owned cats with ORL or not, until late in the interview.

Associations between proposed risk factors and ORL were evaluated using the chi-square test of independence or Fisher’s exact test (where expected cell values were less than 5) for categorical variables, and Student’s t-test for continuous data with a Gaussian distribution.18 The effects of variables significant at a p value of 0.20 or less were evaluated further to control for potentially confounding variables using unconditional logistic regression where the dependent variable was the presence or absence of ORL.19 The model parameters were obtained by maximum likelihood estimation using the computer program EGRET.a The models were constructed using a forward stepwise approach. The assessment of interactions was attempted, but the small sample size resulted in failure to converge in most models. The significance of variables in the models was determined by evaluating the likelihood ratio chi-square statistic in each step of the fitting process. In light of the small numbers, variables significant at a p value of 0.10 or less were retained in the final model. The regression coefficients were exponentiated to obtain the adjusted odds ratio (OR) for each parameter.

Results

Thirty-five cats with ORL and 32 without were identified, of which 33 cases (94%) and 27 controls (84%) were interviewed respectively. Reasons for nonparti-cipation included being too busy, death of a cat, and travel. There were more females in the case group (51.5%) than in the control (40.7%) group, but the difference was not significant. All cats were neutered, and most were of mixed breed (94%). Cases were, on average, a year older than controls, but both groups had been owned an average of 7.5 years and had a mean weight between 11 and 12 pounds [Table 1].

When individual variables were screened for their association with ORL, seven were significant (p value of 0.20 or less). A higher proportion of cats with ORL received two or more brands of canned foods, were fed liver and other organ meats from the table, and had a history of dental disease (including calculus, gingivitis, and periodontal disease). Control cats spent more time outdoors daily (particularly in the summer), lived in rural areas more often, were fed commercial treats more often, and received coat supplements. Control cats were also more likely to have been treated recently for upper respiratory infections (URI), episodes of diarrhea, and to have received antibiotics. When the owners were asked about their respective cat’s medical history, however, there were no differences in the frequency of reported lifetime episodes of URI, diarrhea, or other medical conditions.

The seven factors that were significantly associated with ORL using a liberal p value of 0.20 or less, were examined simultaneously in the multivariate models. Only the four factors that remained significant (p value of 0.10 or less) are discussed. In the multivariate models, four factors (i.e., time spent outdoors, a history of dental disease, urban-rural residence, and consumption of commercial cat treats) remained associated with ORL. Since time spent outdoors was highly correlated with area of residence (i.e., city, village, or rural), both residence and time spent outdoors were not examined in the same multivariate model. Therefore, two models are presented [Table 3]. Living in an urban area (OR, 4.4) and a history of dental disease (OR, 4.5) increased risk more than fourfold compared to cats living on a farm and with no previous dental disease, respectively. Receiving commercial treats reduced risk approximately threefold.

If time spent outdoors was evaluated in lieu of residence, strictly indoor cats had a 4.5 times higher risk of ORL, and cats spending some time (but no more than six hours) outside daily had a 4.3 times higher risk of ORL compared to cats spending seven or more hours outdoors daily in the summer. The risks associated with a history of dental disease and commercial treats were essentially unchanged in this model.

Gender, history of treatment with antibiotics, urinary acidifiers or other medications, source of water supply, number of other cats in the household, frequency of daily feeding, prevalence of free-choice feeding, and the proportion of cats fed canned, dry, or semimoist pet foods were not associated with ORL in this study. Also, consumption of various table foods did not differ significantly between cats with ORL and without ORL.

Discussion

Builder11 first mentioned ORL in 1950, but speculated that the lesions were a form of caries. It wasn’t until 1976 that Schneck first distinguished ORL from dental caries and coined the term “neck lesions.”20 Since that time, the importance of ORL as a leading cause of dental disease in cats has been appreciated. Factors that may predispose cats to the disease are beginning to emerge.

If the apparent increase in ORL prevalence is not just a result of cats living to older ages, then the change suggests the introduction of some environmental factor(s) or the removal of protective ones, or both. The primary objective of this study was to compare exposures to various environmental factors between cats with ORL and without ORL.

Previous dental disease (as recorded in the medical records) was the strongest risk factor identified, with an odds ratio of between four and five (depending on the model), suggesting that cats with previous dental disease had approximately four to five times higher risk for ORL than those without previous dental disease. The prior dental disease was predominantly calculus accumulation, gingivitis, and periodontal disease. One theory of etiopathogenesis suggests that plaque bacteria induce an inflammatory response in the gingival tissue which leads to attraction of circulating stem cells that become odontoclastic cells. These cells then initiate damage and lead to granulation tissue with an enhanced blood supply which facilitates remodeling of bone-cementum tissue, all of which contribute to ORL.21 The inflammation, however, may be secondary to the resorptive lesion.10,20 At least two previous studies have found an association between the occurrence of ORL and periodontitis.7,22

Cats with ORL spent more time indoors, and being indoors most of the time (18 hours or more) increased risk more than fourfold. The converse of this, time outdoors, particularly in the summer, appeared to lower risk. Cats with ORL also spent less time outside during the winter, but the results were not statistically significant, probably reflecting the small number of cats spending prolonged periods outdoors in central New York. The authors speculate that the significance of time spent outdoors may be related to hunting activities and that consuming prey may help to clean teeth and prevent oral disease leading to ORL. Many owners were unsure whether their cat “hunted,” and, therefore, the quality of data solicited with questions regarding hunting is suspect. Lund, et al.,8 found no association with access to the outdoors, but no inquiries were made about time spent outdoors. Access or nonaccess to the outdoors was also not significant in this or a previous study.17 It was only after inquiries were made about time spent outdoors that differences emerged. There are reports of stray and feral cat populations having a lower prevalence of lesions,10 but more studies are needed. The demonstration of ORL in wild felidae23 does not necessarily contradict this hypothesis, as the actual prevalence of wild animals with lesions has not been reported. The finding that some breeds may have a higher prevalence of ORL10 may be a reflection, at least partially, of their lack of access to the outdoors because owners do not want to risk losing valuable animals. There were insufficient purebred cats in this study to evaluate breed as a risk factor.

The increased risk associated with urban residence or, conversely, the protective effect of rural residence (which appeared to decrease risk more than four times compared to city residence) may also be associated with hunting activities. Time spent outdoors and rural residence were significantly associated. It is also possible that some other factor(s) associated with rural residence (such as water source) may be of etiological significance. Lending support to this hypothesis is Lund, et al.’s, observation that a higher proportion of cats with ORL drank well water (according to their univariate analysis).8 Similarly, strictly indoor, city-dwelling cats may be exposed to unknown factor(s) that increase their risk.

The significance of the apparent protective effect of commercial treats is unknown. Approximately 41% of cats with no lesions and 21% of those with lesions received treats at least once weekly. Closer examination of this data revealed that most of the cats with and without ORL which were fed treats received one brand, but the significance of this observation is unclear. It may be that some other aspect of the care or management of cats fed treats is related to risk for ORL, or the finding occurred by chance.

The observation that cats without ORL were more likely to have been treated recently for URI and diarrhea most likely reflects a bias in control selection; that is, when these cats were presented for treatment of URI or another presenting health concern, dental cleanings were recommended. When owners were asked about their respective cat’s history of respiratory, intestinal, and other illnesses, there were no differences between cases and controls. No associations were found with gender, number of cats owned, a history of hair ball regurgitation, prior URI or other diseases, types of diet (e.g., dry or canned), or consumption of various table foods.

While the authors attempted to collect information about potential causes preceding the diagnosis of ORL, the critical period during which the lesions may be induced is unknown. Therefore, data regarding diet, residence, time spent outdoors, etc., was collected primarily from the time of diagnosis of ORL or the time of recommended dental procedures in controls. Since much of the exposure data was cross-sectional in nature (i.e., collected at the time of diagnosis), the design is considered cross-sectional despite sampling cases and controls.

This design enabled the study of multiple possible risk factors but was limited by its cross-sectional nature. The study was also limited by incomplete records, where specific information was either incomplete or entirely missing. Identification of the nature and extent of previous dental disease, for example, was not always complete. Similarly, although every effort was made to remove cats with previous ORL from the control series, a few may have had lesions themselves as not all cats were radiographed. The relatively small sample size also hampered efforts to examine multiple variables simultaneously.

Conclusion

Data from previous studies suggests that the prevalence of feline ORL has increased, possibly due to a change(s) in the environment of cats. Numerous hypotheses have been advanced, but the etiology of these lesions remains elusive. Results from this study suggest that cats spending more time outdoors or living in a rural residence, or both, may have reduced risk, perhaps because of access to supplementation of their diet with natural prey. A decreasing number of cats with outdoor access may explain the increase in frequency of this disease. The etiology is undoubtedly complex, resulting from the ininteraction of multiple factors. In light of its high frequency and serious consequences, further research is warranted.


a Egret Statistical Package User’s Manual, 1987; Statistics and Epidemiology Research Corporation (SERC) Software Division, Seattle, WA



References

1. Ohba S, Kiba H, Kuwabara M, et al. A histopathological study of neck lesions in feline teeth. J Am Anim Hosp Assoc 1993;29:216–20.

2. Harvey CD. Feline resorptive lesions. Sem Vet Med Surg 1993;8:187–96.

3. Frost P, Williams CA. Feline dental disease. Vet Clin N Am Sm Anim Prac 1986;16:851–73.

4. DeBowes LJ. Odontoclastic resorptive lesions in cats. Waltham Focus 1994;4:2–8.

5. Eisner ER. Chronic subgingival tooth erosion in cats. Vet Med 1989;84: 378–87.

6. Lyon KF. Subgingival odontoclastic resorptive lesions. Classification, treatment, and results in 58 cats. Vet Clin N Am Sm Anim Prac 1992;22:1417–32.

7. Van Wessum R, Harvey CE, Hennet P. Feline dental resorptive lesions. Vet Clin N Am Sm Anim Prac 1992;22:1405–15.

8. Lund EM, Bohacek LK, Dahlke JL, et al. Prevalence and risk factors for odontoclastic resorptive lesions in cats. J Am Vet Med Assoc 1998;212: 392–5.

9. Coles S. The prevalence of buccal cervical root resorptions in Australian cats. J Vet Dent 1990;7:14–6.

10. Wiggs RB, Lobprise HB. Veterinary dentistry: principles and practice. Philadelphia: Lippincott-Raven, 1997:487–90.

11. Builder PL. Opening paper. Vet Rec 1955;67:386–90.

12. Okuda A, Harvey CE. Etiopathogenesis of feline dental resorptive lesions. Vet Clin N Am Sm Anim Prac 1992;22:1385–403.

13. Mulligan TW. Feline cervical line lesions. Vet Med Report 1990;2:343–9.

14. Thompson RR, Wilcox GE, Clark WT, et al. Association of calicivirus infection with chronic gingivitis and pharyngitis in cats. J Sm Anim Pract 1984;25:207–10.

15. Zetner K, Steurer I. The influence of dry food on the development of feline neck lesions. J Vet Dent 1992;9:4–6.

16. Seawright AA, English PB, Gartner RJW. Hypervitaminosis A of the cat. Adv in Vet Sci and Comp Med, 1970;14:1–27.

17. Donoghue S, Scarlett JM, Williams CA, et al. Diet as a risk factor for feline external odontoclastic resorption (abstract). J Nutr 1994;124:2693S–4S.

18. Dawson-Saunders B, Trapp RG. Basic and clinical biostatistics. Norwalk, Connecticut: Appleton and Lange, 1994:114–6, 149–55.

19. Kleinbaum DG, Kupper LL, Morgenstern H. Epidemiologic research. London: Lifetime Learning Pub, 1982:461–82.

20. Schneck GW, Osborn JW. Neck lesions in the teeth of cats. Vet Rec 1976;99:100.

21. Harvey CE, Emily PP. Small animal dentistry. St. Louis: Mosby, 1993: 221–5.

22. Harvey CE, Shafer F. Epidemiology of canine and feline oral diseases. Proc Vet Dent Forum 1992;6:45–6.

23. Berger M, Schawalder P, Stich H, et al. Feline dental resorptive lesions in captive and wild leopards and lions. J Vet Dent 1996;13:13–21.
malernee
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VIT D FORL

Postby GUEST » Fri Mar 26, 2004 10:55 pm

There was an article published recently (perhaps around November) by Dr. Alexander Reiter. This article (Evaluation of Serum Concentrations of Calcitropic Hormones in Cats with Feline Odontoclastic Resorptive Lesions.) concludes that cats with FORL had a statistically significant higher 25-hydroxyvitamin D (25OHD) level compared to cats without FORL. There were no diets evaluated in this study. In the discussion section, there are references to a study at UC Davis by Dr. Jim Morris.

As Dr. Reiter points out, there is a need for long term studies in this area.

There are many questions to be answered. As an example, Vitamin D is very difficult to measure in food
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