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It can be challenging to make sure that you get the proper balance of fats, proteins, carbohydrates, and calories while following a ketogenic or low-carb diet. Keep track of macronutrients such as grams of Fat, Protein, and Carbohydrates for a given meal or for an entire day.
The ketogenic diet menu is planned to burn fat and taking control of the metabolism of the body.
Ketogenic diet menu changes can also depend on the age, health and occupation of the person. The ketogenic diet menu provides just enough protein for the repair and growth and right calories to maintain the weight according to height.
Ketogenic diet menu or ketogenic offers snacking on handful of nuts, cheese cubes, celery sticks, low carb tortilla and fresh fruits. The main thing to remember is to check the carbohydrate content that one eats especially of chesses and sauces. Low fat foods should be avoided because after low carb diet, fat is a must to give energy and prevent metabolism.
Butter and oil in cooking should be used freely.  It is seen that in low fat alternatives the fat is replaced by carbohydrates. Frying should be done in non-hydrogenated oils ghee or coconut oil as they have a higher smoke point than other fats. My modified Ketogenic diet plan: Please let me emphasize that this is the plan I worked out for my son and it worked for him. Kiran loves goat milk, which is a dairy product but if you are allergic, dairy intolerant, or just avoiding dairy as in a vegan diet, then substitute with nut based milks or soy (yuck!). If you are fine with dairy, then go ahead and make your own milk by mixing cream and water, so you have a higher fat content milk. Snacks  – Carrots, celery, cucumbers, dipped in nut butters, roasted vegetable dip, tomato chutney dip, my nut free pesto (click here) and salsa (click here).
If you are trying to lose weight or get healthier with Ketosis, here’s a list of the best Ketogenic Diet Foods to add to your menu. Malignant brain cancer persists as a major disease of morbidity and mortality in adults and is the second leading cause of cancer death in children. Adult mice were implanted orthotopically with the malignant brain tumors and KetoCal® was administered to the mice in either unrestricted amounts or in restricted amounts to reduce total caloric intake according to the manufacturers recommendation for children with refractory epilepsy.
The results indicate that KetoCal® has anti-tumor and anti-angiogenic effects in experimental mouse and human brain tumors when administered in restricted amounts. Malignant brain cancer persists as a major disease of morbidity and mortality in adults and is the second leading cause of cancer death in children [1-4]. In this study we evaluated the therapeutic efficacy of KetoCal®, a new nutritionally balanced soybean oil ketogenic diet that was formulated specifically for managing refractory epilepsy in children [34].
The syngeneic mouse brain tumor CT-2A, was originally produced by implantation of a chemical carcinogen, 20-methylcholanthrene, into the cerebral cortex of B6 mice and was characterized as an anaplastic astrocytoma [37,38]. The mouse CT-2A and human U87 tumors were implanted into the cerebral cortex of the B6 or SCID mice, respectively, using a trocar as we previously described [41].
For the survival studies, CT-2A or U87 flank-grown tumors were removed from B6 or SCID mice, respectively, and were rinsed and diced in cold phosphate-buffered saline (PBS) at pH 7.4. The mice were group housed prior to the initiation of the experiment and were then individually housed in plastic shoebox cages one day before tumor implantation. The animal room was maintained at 22 ± 1°C, and cotton nesting pads were provided for additional warmth.
Blood was collected from mice on the last day of the experiment (between 1 - 4 pm) and before sacrifice and tumor resection. Tumor sections were incubated with trypsin at 37°C for 30 min after deparaffinization, rehydration, and washing as we described recently [10,11].
Total RNA was isolated from homogenized tissue using TRIzol Reagent (Invitrogen, La Jolla, CA), following the manufacturers protocol. The one-way analysis of variance (ANOVA) was used to analyze body weight, tumor growth, plasma glucose, and ?-OHB levels [53].
The objective of this study was to determine if the KetoCal® ketogenic diet could be therapeutic against experimental mouse and human brain tumors when administered in restricted amounts according to recommendations for treatment of children with refractory epilepsy.
A transition from glucose to ketone bodies for energy under caloricaly restricted conditions is known to inhibit brain tumor growth through multiple integrated systems [5,9-11]. To determine if KetoCal® influenced angiogenesis, we used Factor VIII immunostaining to examine blood vessel densities in the CT-2A and U87 brain tumors. ?-OHBDH and SCOT are required for the metabolism of ketone bodies for energy in brain mitochondria [13,20,21]. We found that KetoCal®, a nutritionally balanced and commercially available ketogenic diet for children with epilepsy, significantly reduced the orthotopic growth and the vascularity of the mouse astrocytoma (CT-2A) and the human glioma (U87). Although we previously showed that CR of a high carbohydrate standard diet or of a rodent ketogenic diet similarly reduce blood glucose levels, which tumor cells depend upon for survival [10,11], our findings in this study showed that administration of KetoCal® under restricted conditions was more effective in elevating circulating ketone bodies than was administration under unrestricted conditions. Previous studies indicate that many tumors including brain tumors are largely unable to metabolize ketone bodies for energy due to various deficiencies in one or both of the key mitochondrial enzymes, ?-OHBDH and SCOT [19,21,65-68]. Long-term management of malignant brain cancer has been difficult in both children and adults. Although Nebeling and co-workers were successful in managing childhood astrocytoma with a medium-chain triglyceride ketogenic diet [29,73], this KD formulation can be difficult to implement, is not standardized, and can produce some adverse effects as previously observed in children taking the diet for epilepsy management [32-34]. Guidelines for the implementation of KetoCal® and other calorie restricted KDs in younger and older patients have been described previously [5,29,34,73].
I switch around the vegetable options between asparagus, green peas, pumpkin, cauliflower and tomatoes. Have you found that allowing Lentils and Beans (chick peas) etc – still allows for the Ketogenic state? After following a strict ketogenic diet for our son, we slowly increased his carb consumption, while monitoring his epilepsy.
You can keep these in the fridge for kids to munch on, pack them in your lunch and have a bite between two meetings or bring them in your purse for your shopping spree!
An app that could scan your food label and tell you instantly how many net carbs each one of your favorite food contains.
I made this with extra virgin coconut oil, which is one of the healthiest oils (benefits of coconut oil) you can find on top of giving it this little extra yummy Asian taste. Scientists proved that doubling the amount of recommended daily allowance (RDA) of protein while following a diet and exercising. It is very easy and fast to make, it’s low carbs, it fills me up and it’s healthy and DELICIOUS! Many current therapies for malignant brain tumors fail to provide long-term management because they ineffectively target tumor cells while negatively impacting the health and vitality of normal brain cells. The effects KetoCal® on tumor growth, vascularity, and mouse survival were compared with that of an unrestricted high carbohydrate standard diet.
The restricted KetoCal® diet reduced plasma glucose levels while elevating plasma ketone body (?-hydroxybutyrate) levels. The therapeutic effect of KetoCal® for brain cancer management was due largely to the reduction of total caloric content, which reduces circulating glucose required for rapid tumor growth. Many current therapies for malignant brain tumors are ineffective in providing long-term management because they focus on the defects of the tumor cells at the expense of the health and vitality of normal brain cells [5-7]. These enzymes become critical when neurons and glia transition to ketone bodies in order to maintain energy balance under conditions of reduced glucose availability.
The findings in human pediatric astrocytoma were confirmed in the experimental mouse CT-2A astrocytoma using a lard-based rodent ketogenic diet [8,9]. No prior studies have evaluated the therapeutic efficacy of KetoCal® for brain cancer management. The mice were propagated in the animal care facility of the Department of Biology, Boston College, using animal husbandry conditions described previously [36]. The morphological, biochemical, and growth characteristics of the CT-2A mouse brain tumor were previously described [37,39-42]. Influence of diet on body weight in B6 mice bearing the mouse CT-2A astrocytoma (A), and in SCID mice bearing the human U87 glioma (B).
All mice were fasted for 2 hours before blood collection to stabilize blood glucose levels. The Fishers PLSD test was used to calculate two-sided pair-wise comparison among different test groups by use of Statview 5.0.
In contrast to other ketogenic diet formulations (lard-based or medium chain triglyceride diets), which are not standardized or commercially available, KetoCal® is a nutritionally complete medical food for children that would be widely available for alternative indications such as malignant brain cancer. The restriction of KetoCal® in the KC-R group was according to the manufacturers recommendation for the management of childhood epilepsy (Nutricia North America).
Influence of diet on the intracerebral growth of the CT-2A (A) and the U87 (B) brain tumors.
Plasma glucose levels were significantly lower in the KC-R mouse groups than in the SD-UR or the KC-UR groups (Figure 4A and 4B). Influence of diet on plasma glucose and ?-OHB levels in B6 mice bearing the CT-2A astrocytoma (A and C), or in SCID mice bearing the human U87 glioma (B and D).

Influence of diet on vascularity in the CT-2A (A and B) and the U87 (C) brain tumors grown orthotopically in B6 or SCID mice, respectively. Expression of ?-OHBDH and SCOT in B6 and SCID mouse brains and in CT-2A and U87 brain tumors.
This is important since mild ketosis, under conditions of reduced glucose availability, is essential for enhancing the bioenergetic potential of normal brain cells [5,17,18]. Our gene expression results in the mouse CT-2A and the human U87 brain tumors are consistent with these previous findings in other tumors and also support the mitochondrial defect theory of cancer [5,23,24,69].
This has been due in large part to the unique anatomical and metabolic environment of the brain that prevents the large-scale resection of tumor tissue and impedes the delivery of chemotherapeutic drugs. It is noteworthy that the children treated in the Nebeling study also expressed reduced blood glucose levels [29].
KetoCal® could be administered to patients with brain tumors at medical centers or clinics currently using the ketogenic diet for managing epilepsy. It involves a tasty fulfilling diet that is based on meats, vegetables, nuts, beans and healthy fats. The diet excludes foods that are high in carbohydrates like starchy fruits and vegetables, bread, pasta, and sugar and adding foods rich in fat like butter and cream.
One has just to keep in mind that one needs to lower the caloric intake, the fat consumption and the carbohydrates.
If you’d like to find more Keto Recipes to custom your own, take a look at my Ketogenic Diet recipes database.
This will keep you full and will avoid insulin level roller coasters, meaning that it will help you lose weight and save you from that usual energy crash a lot of people experience in the afternoon.
We get into some crazy schedule, running between two appointments, staying late at work or being on the road and we have no time to cook. In contrast to brain tumor cells, which lack metabolic flexibility and are largely dependent on glucose for growth and survival, normal brain cells can metabolize both glucose and ketone bodies for energy. Tumor microvessel density was less in the calorically restricted KetoCal® groups than in the calorically unrestricted control groups.
A dependency on glucose for energy together with defects in ketone body metabolism largely account for why the brain tumors grow minimally on either a ketogenic-restricted diet or on a standard-restricted diet. We previously showed that caloric restriction (CR) is anti-angiogenic, anti-inflammatory, and pro-apoptotic in the experimental mouse (CT-2A astrocytoma) and the human (U87-MG malignant glioma) brain tumors [8-11]. In addition to serving as a more efficient metabolic fuel than glucose, ketone bodies also possess anti-inflammatory potential through reduction of reactive oxygen species and increase of glutathione peroxidase activity [5,17,22]. CR and some KDs, however, are not standardized diets and may be difficult to implement in the clinic due to issues of compliance. Here we show that KetoCal®, given in calorically restricted amounts significantly reduced circulating plasma glucose levels while significantly elevating ketone body levels in mice bearing orthotopic CT-2A and U87-MG brain tumors. Male mice (10 - 12 weeks of age) were used for the studies and were provided with food under either restricted or unrestricted conditions (as below). The U87-MG (U87) tumor was originally derived from a human malignant glioma cell line and was grown as a xenograft in the SCID mice [43,44].
Louis, MO) given intra-peritoneally and their heads were shaved and swabbed with 70% ethyl alcohol under sterile conditions. The flanks of recipient mice were shaved in order to facilitate tumor detection and growth assessment. This is a standard high carbohydrate mouse chow diet (SD) and contains a balance of mouse nutritional ingredients. Survival was determined as the time for subcutaneous tumors to reach the size of 2.5 cm3 after tumor inoculation as previously described [45]. The mice were anesthetized with isoflurane (Halocarbon, NJ), and the blood was collected from the heart into heparinized tubes. Single-strand cDNA was synthesized from total RNA (3 ?g) by using oligo (dT) primers (Promega, Madison, WI) in a 20-?l reaction with Moloney murine leukemia virus reverse transcriptase (M-MLV RT; Promega) according to the manufacturers protocol. Because we previously showed that CR of the high carbohydrate standard diet has anti-tumor and anti-angiogenic effects against the CT-2A and U87 experimental brain tumors [10,11], we did not include a hypocaloric group for the high carbohydrate diet in this study. This involved administration of 65 - 70% recommended daily allowance of calories or an approximate 30 - 35% calorie restriction.
It is important to mention that all implanted CT-2A and U87 tumors grew in the KC-R groups, indicating that restricted feeding did not prevent tumor "take" but significantly reduced the intracerebral growth rate. The number of blood vessels in the CT-2A tumor was noticeably less in the KC-R group than in the SD-UR group (Figure 5A). Vessels were stained with the Factor VIII antibody and each stained section was representative of the entire tumor.
?-OHBDH and SCOT mRNA levels were significantly lower in the CT-2A and the U87 tumor tissue than in the normal appearing contralateral brain tissue.
It is important to mention that the anti-angiogenic and growth inhibitory effects of KetoCal® were observed only when the diet was administered in restricted amounts but were not seen when the diet was administered ad libitum, or in unrestricted amounts.
Additionally, ketone bodies may directly protect normal neurons and glia from damage associated with aggressive tumor growth through a variety of neuroprotective mechanisms [59-64]. The deficiencies in these enzymes, however, are important for tumor management only under calorically restricted conditions when glucose levels are reduced and when cells would require ketone bodies for energy.
Further, significant neurological abnormalities are often observed in long-term brain tumor survivors [70-72]. When administered in restricted amounts, KetoCal® may have greater therapeutic efficacy with fewer side effects than medium-chain triglyceride or lard-based KDs. It is an effective diet for burning of fat and also as a treatment for some neurological conditions. If avoiding dairy and are leery of nut-based milks because of allergies, try coconut milk and coconut cream for topping cereals and making hot drinks like cocoa or even coffee (for adults). I suggest using organic, extra virgin coconut oil for this recipe (I like Nutiva) which is an amazing source of fat that helps your cholesterol levels (read about the health benefits of coconut oil by Dr Oz). Keto is a low carbohydrate diet that is used not only to lose weight but also to treat and prevent cancer, epilepsy, Alzheimer and other diseases.
Moreover, gene expression for the mitochondrial enzymes, ?-hydroxybutyrate dehydrogenase and succinyl-CoA: 3-ketoacid CoA transferase, was lower in the tumors than in the contralateral normal brain suggesting that these brain tumors have reduced ability to metabolize ketone bodies for energy. CR targets tumor cells by reducing circulating glucose levels and glycolysis, which tumor cells need for survival, and by elevating ketone bodies, which provide normal brain cells with an alternative fuel to glucose [5,9,11]. Brain tumors, like most malignant tumors, are largely dependent on glucose and glycolysis for their growth and survival due to abnormalities in the number and function of their mitochondria [5,8,23-27].
For example, CR in mice mimics therapeutic fasting in humans, involving water-only dieting, whereas medium chain triglyceride or lard-based ketogenic diets can cause gastrointestinal and kidney problems in both children and adults [30-33].
Moreover, the restricted KetoCal® diet reduced brain tumor growth and microvessel density, while extending mouse survival. Small tumor pieces (about 1 mm3) from donor mice were implanted into the right cerebral hemisphere of anesthetized recipient mice as we recently described [41].
For the survival analysis, the dietary treatment was initiated 7 days after subcutaneous implantation and continued until the tumors reached 2.5 cm3. The SD-UR, KC-UR, and KC-R represent the standard high carbohydrate diet fed unrestricted, the KetoCal® diet fed unrestricted, and the KetoCal® diet fed in restricted amounts, respectively. The blood was centrifuged at 1,500 ? g for 10 min, and the plasma was collected and stored at -80°C until assayed. For the histological studies, treatment was initiated as described above and was continued for 7 days to prevent tumor-associated tissue distortion. Consequently, the restricted KetoCal® mouse groups were compared to mouse groups receiving either the standard chow diet or the KetoCal® diet in unrestricted amounts. This degree of dietary restriction gradually produced an approximate 20 - 23% body weight reduction by 11 days post i.c. Survival, assessed as the time required for subcutaneous tumor nodules to reach 2.5 cm3, was significantly longer in the KC-R groups than in the SD-UR or KC-UR groups (Figure 3A and 3B).
These findings are consistent with our previous studies in mice showing that the KD does not lower plasma glucose levels when administered in unrestricted amounts [8,18].
No differences in ?-OHBDH and SCOT mRNA levels were found between normal appearing brain tissue from tumor-bearing mice and brain tissue from non-tumor-bearing mice (data not shown). Expression was evaluated in normal appearing B6 brain tissue (B6-B) contralateral to the CT-2A tumor, and in normal appearing SCID brain tissue (SCID-B) contralateral to the U87 tumor.
These findings support previous observations that restriction of dietary calories has powerful anti-angiogenic and anti-inflammatory effects against cancer, including brain cancer [9-11,51,57,58].
In contrast to most conventional brain tumor therapies, which indiscriminately target both normal cells and tumor cells, CR and particularly restricted ketogenic diets such as KetoCal® are the only known therapies that can target brain tumor cells while enhancing the health and vitality of normal brain cells [5,29].
This is most evident from the analysis of tumor growth in the unrestricted KetoCal® groups where growth was rapid despite mild ketosis.
In light of the differences in energy metabolism between normal brain cells and brain tumor cells, we recently proposed an alternative approach to brain cancer management based on principles of evolutionary biology and metabolic control theory [5].
Additionally, KetoCal® would eliminate or reduce the need for antiepileptic drugs for brain tumor patients since KetoCal® was designed originally to manage refractory epileptic seizures. Hot cooked oatmeal is better than store bought pre-packaged dry cereals and can be topped with coconut milk and sweetened with coconut sugar or pure maple syrup.

You can still stick to your low carb plan as I have some options to help you make the best choice for your situation.
This preclinical study indicates that restricted KetoCal® is a safe and effective diet therapy and should be considered as an alternative therapeutic option for malignant brain cancer.
We previously used linear regression analysis to show that blood glucose levels could predict CT-2A growth as well as insulin-like growth factor 1 (IGF-1) levels, which influences tumor angiogenesis [8,9]. The transition from glucose to ketone bodies as the primary energy source of the brain under calorically restricted conditions exploits the metabolic deficiencies of brain tumor cells while enhancing the health and vitality of normal neurons and glia according to principles of evolutionary biology and metabolic control theory [5,28].
Our goal was to develop a more effective alternative diet therapy for brain cancer that could extend survival without compromising the health and vitality of normal cells. Gene expression for ?-OHBDH and SCOT was lower in the tumors than in contralateral normal brain suggesting that the brain tumors have reduced ability to metabolize ketone bodies for energy.
Initiation of tumors from intact tumor pieces is preferable to initiation from cultured cells, since the tumor tissue contains an already established microenvironment that facilitates rapid tumor growth [41].
The KetoCal® ketogenic diet was obtained as a gift from Nutricia North America (Rockville, MD, formally SHS International, Inc.). Plasma glucose and ?-OHB concentrations were measured spectrophotometrically using the StanBio® Enzymatic Glucose Assay (1075-102) (StanBio Laboratory, Boerne, TX, USA) and a modification of the Williamson et al., enzymatic procedure [47], respectively. Primer sequences and amplicon information for the mouse and the human ?-actin, ?-OHBDH, and SCOT genes can be viewed at NCBI (National Center for Biotechnology Information, PubMed) using the accession numbers EF095208-EF095213.
Survival was computed and plotted according to the nonparametric Kaplan-Meier analysis, and comparison of control and treated groups was made using the log-rank test [53]. No significant differences in survival were found among tumor-bearing mice in the SD-UR or the KC-UR groups. In contrast to glucose levels, circulating ?-OHB levels were 2 to 3-fold greater in the KC-UR groups than in the SD-UR groups (Figure 4C and 4D). As found in the CT-2A tumor, the number of blood vessels in the U87 tumor was noticeably less in the KC-R group than in the SD-UR group (Figure 5C). The values are expressed as the mean of three independent samples with error bars representing SEM. These findings suggest that the CT-2A and the U87 tumor cells are less capable than the normal mouse brain cells in using ketone bodies for energy. Reduced caloric content lowers circulating glucose levels as we found in this study and in our previous studies [10,11]. In this regard, the calorically restricted ketogenic diet for brain cancer management stands apart from all conventional therapeutic approaches.
This is attributed to the maintenance of high glucose levels, which the tumor cells will use for energy in preference to ketone bodies due to their dependency on glycolysis. Specifically, the genomic and metabolic flexibility of normal cells, which evolved to survive under physiological extremes, can be used to target indirectly the genetically defective and less fit tumor cells. Adjuvant steroidal medications, which are often prescribed to brain tumor patients and which can produce severe adverse effects, might also be reduced under the restricted KetoCal® diet since glucocorticoid levels increase naturally under calorically restricted conditions [74-76]. Almond milk (if there aren’t any allergy concerns)  and hemp milk are low carb alternatives. As an occasional treat, try my rice flour pancakes which are vegan and gluten free (link to video). In contrast to glucose, ketone bodies (?-hydroxybutyrate and acetoacetate) bypass glycolysis and directly enter the mitochondria for oxidation [12,13]. This preclinical study indicates that KetoCal® is a safe and effective diet therapy for malignant brain cancer and can be considered as an alternative or adjuvant therapeutic option. All animal experiments were carried out with ethical committee approval in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals and were approved by the Institutional Animal Care Committee. All of the mice recovered from the surgical procedure and were returned to their cages when they appeared fully active. For blood ketone body analysis, we measured only ?-OHB levels because this is the major blood ketone body in plasma [48,49]. Gradient PCR was performed to obtain optimal primer annealing temperatures as previously described [52]. No signs of vitamin or mineral deficiency were observed in the KC-R mice based on standard criteria in mice [54]. These findings indicate that KetoCal®, administered in recommended restricted amounts, significantly reduced tumor growth and extended survival in mice bearing either the mouse CT-2A or human U87 brain tumors. Interestingly, ?-OHB levels were 5 to 9-fold greater in the KC-R groups than in the SD-UR groups. The values are expressed as the mean of three-four independent samples with error bars representing SEM.
Indeed, tumor growth is more strongly correlated with circulating glucose levels than with circulating ketone body levels [8].
However, when glucose becomes limited, as occurs under CR, the SCOT and ?-OHBDH deficiencies would prevent tumor cells from using ketones as an alternative fuel thus metabolically isolating the tumor cells from the normal cells.
The results of this study using restricted KetoCal® as a therapy for experimental brain cancer provide direct support for this alternative approach to brain cancer management. Ketogenic diets and calorically restricted diets can also antagonize cancer cachexia [9,11,77]. The ketogenic plan has no repetition of meals;   there is enough choice of foods to choose from. By bypassing glycolysis, ketone bodies are also effective for treatment of inherited defects in glucose transporters and pyruvate dehydrogenase, which connects glycolysis with respiration [14-16].
In order to determine the optimal linear range for semi-quantitative RT-PCR, PCR was performed at increasing cycle numbers. Indeed, physical activity and grooming behavior was noticeably greater in the KC-R groups than in the SD-UR and KC-UR groups. These findings are also consistent with our previous studies in mice showing that circulating ?-OHB levels are greater under restricted than unrestricted dietary conditions [8,18,55,56]. No differences in the number or density of blood vessels were observed between the SD-UR and KC-UR groups for either tumor (data not shown). The reduction in glucose levels following restriction of dietary calories largely accounts for why tumors grow minimally on either restricted ketogenic diets or on restricted high carbohydrate standard diets. We suggest that the genes for these enzymes could be useful markers for screening brain tumors and other tumor types that may be responsive to therapy using restricted KetoCal® or other restricted ketogenic diets. It should be recognized that this alternative therapeutic approach may not be restricted only to brain cancer, but could also be effective for any cancer types containing genetically compromised and metabolically challenged tumor cells. These observations, considered together with the anti-angiogenic effects of the diet, suggest that the restricted KetoCal® diet can manage brain tumors through multiple integrated systems.
Microvessel density was quantified by examining areas of vascular hot spots in high power fields (hpf, 200 ?) as previously described [50] with some modifications [51]. PCR amplification was performed with Taq DNA polymerase (Promega) using similar protocols for each gene. These findings indicate that KetoCal® was well tolerated in tumor-bearing B6 and SCID mice and, when given in restricted amounts, produced noticeable improvement in health and vitality. These findings indicate that KetoCal®, administered in restricted amounts, was anti-angiogenic in the CT-2A and U87 brain tumors. Restriction of calories in humans may be difficult to achieve, however, due to issues of compliance.
Moreover, KetoCal® will be more effective in managing brain tumors in humans than in managing brain tumors in mice since prolonged caloric restriction can be tolerated better in humans than in mice due to intrinsic differences in basal metabolic rate [30]. The transition from glucose to ketone bodies for brain energy metabolism is best under the natural conditions of CR [5,8,18].
Briefly, sections were scanned at 40 ? and at 100 ? for the localization of vascular hot spots. Compliance may be better with KetoCal® as this diet was designed for managing refractory human epilepsy under calorically restricted conditions.
A comparison of the nutritional composition of the SD and the KetoCal® diet is presented in Table 1. Blood vessels were counted at 200 ? in the three most non-necrotic vascular areas of the tumor. For example, a 40% CR diet in mice is comparable to therapeutic fasting in humans, which can be difficult for many people [30]. In addition to reducing circulating glucose levels, a restriction of total calories also reduces potential adverse effects of the high fat content of the diet since energy homeostasis is maximized under CR regardless of caloric origin [8,30]. The restricted KetoCal® diet should therefore be easier to implement than therapeutic fasting for brain cancer patients.

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