Federal and state benefits for transition age youth.

While all children face challenges as they become adults, children with chronic medical conditions or disabilities face unique barriers in their transition to adulthood. Children, especially those who are low income and have special needs, are eligible for a range of supports including income supports, health care coverage, vocational and educational supports. These supports are critical to sound health because they ensure access to necessary medical services, while also offsetting the social determinants that negatively affect health. Unfortunately, as children transition into adulthood, eligibility for these benefits can change abruptly or even end entirely. If medical providers have a better understanding of five transition key dates, they can positively impact their patients' health by ensuring continuous coverage through the transition to adulthood. The key dates are as follows: (1) transition services for students with an Individualized Education Program (IEP) must begin by age 16 (in some states such as Illinois, these services must be in place by age 14 1/2); (2) at age 18, eligibility for income supports may change; (3) at age 19, eligibility for Medicaid may change; (4) at graduation, eligibility for educational supports will end unless steps are taken to extend those benefits until age 22; and (5) when individuals prepare to enter the workforce, they will become eligible for vocational rehabilitation services. With an understanding of these key transition dates and how to partner with social services and advocacy organizations on behalf of their patients, medical providers can help to ensure that transition-age patients retain the holistic social services and supports they need to protect their health.

Different sources of omega-3 polyunsaturated fatty acids affects apparent digestibility, tissue deposition, and tissue oxidative stability in growing female rats.

BACKGROUND: Numerous health benefits associated with increased omega-3 polyunsaturated fatty acid (n-3 PUFA) consumption has lead to an increasing variety of available n-3 PUFA sources. However, sources differ in the type, amount, and structural form of the n-3 PUFAs. Therefore, the objective of this study was to determine the effect of different sources of ω-3 PUFAs on digestibility, tissue deposition, eicosanoid metabolism, and oxidative stability. METHODS: Female Sprague-Dawley rats (age 28 d) were randomly assigned (n = 10/group) to be fed a high fat 12% (wt) diet consisting of either corn oil (CO) or n-3 PUFA rich flaxseed (FO), krill (KO), menhaden (MO), salmon (SO) or tuna (TO) oil for 8 weeks. Rats were individually housed in metabolic cages to determine fatty acid digestibility. Diet and tissue fatty acid composition was analyzed by gas chromatography and lipid classes using thin layer chromatography. Eicosanoid metabolism was determined by measuring urinary metabolites of 2-series prostaglandins (PGs) and thromoboxanes (TXBs) using enzyme immunoassays. Oxidative stability was assessed by measuring thiobarbituric acid reactive substances (TBARS) and total antioxidant capacity (TAC) using colorimetric assays. Gene expression of antioxidant defense enzymes was determined by real time quantitative polymerase chain reaction (RT-qPCR). RESULTS: Rats fed KO had significantly lower DHA digestibility and brain DHA incorporation than SO and TO-fed rats. Of the n-3 PUFA sources, rats fed SO and TO had the highest n-3 PUFAs digestibility and in turn, tissue accretion. Higher tissue n-3 LC-PUFAs had no significant effect on 2-series PG and TXB metabolites. Despite higher tissue n-3 LC-PUFA deposition, there was no increase in oxidation susceptibility indicated by no significant increase in TBARS or decrease in TAC and gene expression of antioxidant defense enzymes, in SO or TO-fed rats. CONCLUSIONS: On the basis that the optimal n-3 PUFA sources should provide high digestibility and efficient tissue incorporation with the least tissue lipid peroxidation, TO and SO appeared to be the most beneficial of the n-3 PUFAs sources evaluated in this study.

Consumption of different sources of omega-3 polyunsaturated fatty acids by growing female rats affects long bone mass and microarchitecture.

Omega-3 polyunsaturated fatty acids (ω-3 PUFAs) consumption has been reported to improve bone health. However, sources of ω-3 PUFAs differ in the type of fatty acids and structural form. The study objective was to determine the effect of various ω-3 PUFAs sources on bone during growth. Young (age 28d) female Sprague-Dawley rats were randomly assigned (n=10/group) to a high fat 12% (wt) diet consisting of either corn oil (CO) or ω-3 PUFA rich, flaxseed (FO), krill (KO), menhaden (MO), salmon (SO) or tuna (TO) for 8 weeks. Bone mass was assessed by dual-energy X-ray absorptiometry (DXA) and bone microarchitecture by micro-computed tomography (µCT). Bone turnover markers were measured by enzyme immunoassay. Lipid peroxidation was measured by calorimetric assays. Results showed that rats fed TO, rich in docosahexaenoic acid (DHA, 22:6ω-3) had higher (P<0.009) tibial bone mineral density (BMD) and bone mineral content (BMC) and lower (P=0.05) lipid peroxidation compared to the CO-fed rats. Reduced lipid peroxidation was associated with increased tibial BMD (r2=0.08, P=0.02) and BMC (r2=0.71, P=0.01). On the other hand, rats fed FO or MO, rich in alpha-linolenic acid (ALA, 18:3ω-3), improved bone microarchitecture compared to rats fed CO or SO. Serum osteocalcin was higher (P=0.03) in rats fed FO compared to rats fed SO. Serum osteocalcin was associated with improved trabecular bone microarchitecture. The animal study results suggest consuming a variety of ω-3 PUFA sources to promote bone health during the growth stage.

Neurokinin B acts via the neurokinin-3 receptor in the retrochiasmatic area to stimulate luteinizing hormone secretion in sheep.

Recent data have demonstrated that mutations in the receptor for neurokinin B (NKB), the NK-3 receptor (NK3R), produce hypogonadotropic hypogonadism in humans. These data, together with reports that NKB expression increases after ovariectomy and in postmenopausal women, have led to the hypothesis that this tachykinin is an important stimulator of GnRH secretion. However, the NK3R agonist, senktide, inhibited LH secretion in rats and mice. In this study, we report that senktide stimulates LH secretion in ewes. A dramatic increase in LH concentrations to levels close to those observed during the preovulatory LH surge was observed after injection of 1 nmol senktide into the third ventricle during the follicular, but not in the luteal, phase. Similar increases in LH secretion occurred after insertion of microimplants containing this agonist into the retrochiasmatic area (RCh) in anestrous or follicular phase ewes. A low-dose microinjection (3 pmol) of senktide into the RCh produced a smaller but significant increase in LH concentrations in anestrous ewes. Moreover, NK3R immunoreactivity was clearly evident in the RCh, although it was not found in A15 dopaminergic cell bodies in this region. These data provide evidence that NKB stimulates LH (and presumably GnRH) secretion in ewes and point to the RCh as one important site of action. Based on these data, and the effects of NK3R mutations in humans, we hypothesize that NKB plays an important stimulatory role in the control of GnRH and LH secretion in nonrodent species.

Determination of digestibility, tissue deposition, and metabolism of the omega-3 fatty acid content of krill protein concentrate in growing rats.

Krill protein concentrate (KPC) consists of high-quality protein (77.7% dry basis) and lipids (8.1% dry basis) that are rich (27% of total fatty acids) in omega-3 polyunsaturated fatty acids (omega-3 PUFAs). The objective of the study was to determine digestibility, tissue deposition, metabolism, and tissue oxidative stability of the omega-3 PUFAs provided by KPC. Young female Sprague-Dawley rats (n = 10/group) were fed ad libitum isocaloric diets for 4 weeks with either 10% freeze-dried KPC or 10% casein. The casein diet contained 5.3% added corn oil (CO), whereas the KPC contained 5.3% total lipids from 0.9% krill oil (KO) provided by KPC and 4.4% added corn oil (KO + CO). Fatty acid compositions of various tissues were analyzed by gas chromatography. Lipid peroxidation was determined by thiobarbituric acid reactive substances (TBARS). Total antioxidant capacity and urinary eicosanoid metabolites were determined by enzyme immunoassay. The omega-3 PUFAs provided in KO from KPC increased (P = 0.003) docosahexaenoic acid (DHA) concentration in the brain. DHA and eicosapentaenoic acid (EPA) content in fat pads and liver were increased (P < 0.01), whereas the omega-6 PUFA, arachidonic acid (AA), was decreased (P < 0.01) in rats fed the KPC diet containing the KO + CO mixture compared to rats fed the casein diet containing pure CO. Feeding the KPC diet decreased pro-inflammatory 2-series prostaglandin and thromboxane metabolites. There was no significant difference in TBARS or total antioxidant capacity in the tissues of rats fed the different diets. On the basis of the study results, the low amount of omega-3 PUFAs provided by the KO content of KPC provides beneficial effects of increasing tissue EPA and DHA deposition and reduced AA-derived 2-series eicosanoid metabolites without increasing lipid peroxidation. Therefore, consumption of KPC has the potential to provide a healthy and sustainable source of omega-3 PUFAs.