1

2015 Newsletter Editor:

Donna Otero

4975 Friendly Farms Road

Greensboro, NC 27406

dotero7965@gmail.com

GMKC by-laws state that the newsletter is to

be distributed 2 weeks IN ADVANCE OF THE

GENERAL MEETING. Therefore, ALL articles

and information for the newsletter need to be

submitted by the TUESDAY that is 2 WEEKS

FOLLOWING THE GENERAL MEETING. For

the December 2015 newsletter, I will need

all your information by November 24, 2015.

Opinions expressed in this newsletter are

those of the contributor and do not necessarily

reflect the views of GMKC either as a group or

individually.

Advice or helpful hints should never be taken

as substitutes for personal veterinary counsel.

Contact and referral persons are in no way

guaranteed by the GMKC

2015 Officers and Directors

President—John Schoeneman

Vice President—Martha Milligan

Secretary—Janet Broome

Treasurer— Gene Hains

Board of Directors

Beth Warren

Lynn Rowell

Pat Ginocchio

December 2015 Newsletter

www.greatermonroekc.org Page

GMKC Christmas Party

(In lieu of December General Meeting)

December 9, 2015 at 6:30pm

Rolling Hills Country Club

2722 Roosevelt Blvd. Monroe NC

Please RSVP to Martha Milligan mmilligan@earthlink.net by Friday, December 4.

Bring a wrapped gift for the

Chinese Gift Exchange

&

A Wrapped Gift for our Turning Point Families

Please see our Turning Point

Families’ Wish List

On the following Page

Menu: Dry Rubbed NY Strip Loin, Spinach and Cranberry

Stuffed Pork Loin with Bourbon Glaze, Jerk Seasoned Salmon

over Apple "Slaw", Sautéed Green Beans Amandine, Whipped

Yukon Gold Potato, Salad Bar and Hot Fudge Cobbler.

Inside this edition:

Christmas Party Info Page 1

Turning Point Families Page 2

GMKC Nov. Meeting Minutes Page 3

Karen’s Korner Page 5

2

GMKC Paw Prints December 2015

www.greatermonroekc.org Page

Client 1: Ana

Age: 37

SIZES:

Dress: XL

Pants: 14/16

Shirt: XL

Shoes: 9

Special Wish: Perfume,

Shoes, Makeup (L’oreal

True Match W55 Sun-

tan), Nail Polish

Child Name: Bryan

Age: 12

SIZES:

Pants: 18

Shirt: L/XL

Shoes: 8 1/2

Special Wish: Jogging

pants, Sneakers, Foot-

ball, Coat, Clothes, Mov-

ie Tickets (Sun Valley 14

Indian Trail)

Child Name: Steven

Age: 9

SIZES:

Pants: 8

Shirts M

Shoes: 2 1/2

Special Wish: Basket-

ball, Football Sneakers,

Pajamas, Clothes, Coat

Movie Tickets (Sun Val-

ley 14 India Trail

Client 2: Dolores

Age: 50

SIZES:

Pants: L

Shirt: XL

Shoes: 8

Special Wish: Exercise Outfit (Pants L, Tops

XL), Visa Gift Card (in the process of loosing

weight will need to purchase clothes)

3

www.greatermonroekc.org Page

Page

GMKC Paw Prints December 2015

GMKC MEETING/BOARD MINUTES – December 10, 2014

Meeting called to order at 8:05 p.m.

The December meeting was held at Rolling Hills Country Club, Monroe, NC. It is the annual Christmas Banquet

and business items were brief for this meeting.

Secretary’s Minutes: Motion to approve minutes from last meeting made by Martha Milligan, second by Betty

Montgomery.

Treasurer’s Report: We have opened the club account at Bank of America. Any checks written on the BB&T

account should be presented soon since that account will be closing.

We have made the first payment on the Cabarrus County property. We have had the grounds mowed and the

shrubbery has been trimmed. We paid a landscaper/gardener (recommended by Beth Warren) $100 to mow,

trim and tidy up the grounds.

Pet Safe Report: We have one dog, a pit bull, who is being boarded through the holidays.

Membership Report: Membership dues are $20, individual, $25 for family and are due. Please pay your club

dues this month. Notices for dues to be paid will be sent out around the end of year/first of year. They are due

January 1, 2015.

Officers for Club for 2015: The Secretary cast the vote for the club electing the following officers for the 2015

Club Year:

President: John Schoeneman

Vice President: Martha Milligan

Treasurer: Gene Hains

Secretary: Janet Broome

Board Member: Lynn Rowell

We need to designate one of the board members to be Membership Chairman for the Club Year 2015.

New Business: Show Committee Meeting is scheduled for December 29, 6:00 p.m., Martha Milligans. We have

a number of items from the November show to discuss and items to get ready for March 2015 show.

Meeting Adjourned 8:19 p.m.

No Board Meeting tonight.

End of Report

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IT’S TIME TO PAY THOSE CLUB DUES

Please send in your Membership Dues by the end of the year

$20.00 per Individual

$25.00 per Household

Send to Bobbe Jackson: 5913 Rocky River Road, N., Indian Trail, NC 28079

5

All articles in this section were

submitted by Karen Phillips

Don’t Neuter

Your Dog Just

Yet

Review of

Seizures/

Epilepsy in

Animals

Penn/Baylor

Study of Underly-

ing Cause of Dia-

betes in Dogs

Spay Neuter or Shot

How and Injection

Could be the Future

of Animal Control

6

Don’t Neuter Your Dog YET – Read This Life-

Saving Information First!

A very legitimate concern, pet overpopulation, has been the primary driving force behind 30 years of

national and local spay/neuter campaigns.

When it comes to deciding at what age a companion animal should be sterilized, the standard for

most spay/neuter campaigns has been sooner rather than later. This is especially true in the case of

adoptable abandoned and rescued pets that wind up in shelters and foster care.

Recently, however, some animal health care experts have begun to question whether early steriliza-

tion is a good idea for every pet.

Dr. Alice Villalobos, a well-known pioneer in the field of cancer care for companion animals, asks the

question:

"But what if large-scale studies found that early neutering jeopardizes the health of our pets?"

"What if we found enough epidemiological evidence that early neutering of pet dogs may open them

to orthopedic, behavioral, immunologic and oncologic issues?"

Back in 1977, Dr. Villalobos founded a rescue organization called the Peter Zippi Fund for Animals,

which has to date rescued and re-homed nearly 12,000 pets. Her organization was one of thou-

sands that looked at the tragic situation in U.S. shelters and determined early spay/neuter was the

best way to lessen the suffering and ultimate euthanasia of so many feral and abandoned animals.

As a veterinary oncologist and founder of the pet hospice program Pawspice, Dr. Villalobos con-

cedes, "It is earth shattering to consider that some of the cancers we have been battling may have

been enhanced by early neutering instead of the reverse."

Dr. Becker's Comments:

It's unfortunately true that a growing body of research is pointing to early sterilization as the common

denominator for development of several debilitating and life-threatening canine diseases.

On one hand, we certainly want to know what's causing our precious canine companions to develop

disease. On the other hand, it's troubling to learn a procedure we've historically viewed as life-saving

and of value to the pet community as a whole, has likely played a role in harming the health of some

of the very animals we set out to protect.

The same amount of evidence has not been compiled for early spay/neuter of cats, but it's not clear

how well the subject is being studied for kitties. Funding for research into feline health issues falls

well below dollars allocated for their canine counterparts.

Cardiac Tumors

A Veterinary Medical Database search of the years 1982 to 1995 revealed that in dogs with tumors

of the heart, the relative risk for spayed females was over four times that of intact females.

7

For the most common type of cardiac tumor, hemangiosarcoma (HAS), spayed females had a great-

er than five times risk vs. their intact counterparts. Neutered male dogs had a slightly higher risk

than intact males.

The study concluded that, "… neutering appeared to increase the risk of cardiac tumor in both sex-

es. Intact females were least likely to develop a cardiac tumor, whereas spayed females were most

likely to develop a tumor. Twelve breeds had greater than average risk of developing a cardiac tu-

mor, whereas 17 had lower risk."

Bone Cancer

In a study of Rottweilers published in 2002, it was established the risk for bone sarcoma was signifi-

cantly influenced by the age at which the dogs were sterilized.

For both male and female Rotties spayed or neutered before one year of age, there was a one in

four lifetime risk for bone cancer, and the sterilized animals were significantly more likely to develop

the disease than intact dogs of the same breed.

In another study using the Veterinary Medical Database for the period 1980 through 1994, it was

concluded the risk for bone cancer in large breed, purebred dogs increased twofold for those dogs

that were also sterilized.

Prostate Cancer

It's commonly believed that neutering a male dog will prevent prostatic carcinoma (PC) – cancer of

the prostate gland.

But worthy of note is that according to one study conducted at the College of Veterinary Medicine at

Michigan State University, "…castration at any age showed no sparing effect on the risk of develop-

ment of PC in the dog."

This was a small study of just 43 animals, however. And researchers conceded the development of

prostate cancer in dogs may not be exclusively related to the hormones produced by the testicles.

Preliminary work indicates non-testicular androgens exert a significant influence on the canine pros-

tate.

Abnormal Bone Growth and Development

Studies done in the 1990's concluded dogs spayed or neutered under one year of age grew signifi-

cantly taller than non-sterilized dogs or those not spayed/neutered until after puberty. And the earlier

the spay/neuter procedure, the taller the dog.

Research published in 2000 in the Journal of Pediatric Endocrinology and Metabolism may explain

why dogs sterilized before puberty are inclined to grow abnormally:

At puberty, estrogen promotes skeletal maturation and the gradual, progressive closure of the epi-

physeal growth plate, possibly as a consequence of both estrogen-induced vascular and osteo-

blastic invasion and the termination of chondrogenesis.

In addition, during puberty and into the third decade, estrogen has an anabolic effect on the osteo-

blast and an apoptotic effect on the osteoclast, increasing bone mineral acquisition in axial and ap-

pendicular bone.

8

It appears the removal of estrogen-producing organs in immature dogs, female and male, can cause

growth plates to remain open. These animals continue to grow and wind up with abnormal growth

patterns and bone structure. This results in irregular body proportions.

According to Chris Zink, DVM:

"For example, if the femur has achieved its genetically determined normal length at 8 months when

a dog gets spayed or neutered, but the tibia, which normally stops growing at 12 to 14 months of

age continues to grow, then an abnormal angle may develop at the stifle. In addition, with the extra

growth, the lower leg below the stifle likely becomes heavier (because it is longer), and may cause

increased stresses on the cranial cruciate ligament."

Higher Rate of ACL Ruptures

A study conducted at Texas Tech University Health Sciences Center on canine anterior cruciate lig-

ament (ACL) injuries concluded that spayed and neutered dogs had a significantly higher incidence

of ACL rupture than their intact counterparts. And while large breed dogs had more ACL injuries,

sterilized dogs of all breeds and sizes had increased rupture rates.

Hip Dysplasia

In a retrospective cohort study conducted at Cornell University's College of Veterinary Medicine, and

published in the Journal of the American Veterinary Medical Association, results showed that both

male and female dogs sterilized at an early age were more prone to hip dysplasia.

Other Early-Age Spay/Neuter Health Concerns

Early gonad removal is commonly associated with urinary incontinence in female dogs and has been

linked to increased incidence of urethral sphincter incontinence in males.

Spayed and neutered Golden Retrievers are more likely to develop hypothyroidism.

A cohort study of shelter dogs conducted by the College of Veterinary Medicine at Texas A&M Uni-

versity concluded that infectious diseases were more common in dogs that were sterilized at less

than 24 weeks of age.

The AKC's Canine Health Foundation issued a report pointing to a higher incidence of adverse reac-

tions to vaccines in sterilized dogs.

Among the reports and studies pointing to health concerns associated with early spaying and neu-

tering, you can also find mention of increased incidence of behavioral problems including:

Noise phobias

Fearful behavior

Aggression

Undesirable sexual behaviors

Risks versus Benefits of Early Sterilization

Every important decision in life comes with risks as well as benefits.

9

As responsible animal guardians, I believe we owe it to our pets to make the best health choices we

can for them.

As responsible members of society, we owe it to our communities to proactively protect our intact

pets from unplanned breeding at all costs. We must hold ourselves to the highest standard of repro-

ductive control over the intact animals we are responsible for.

Clearly, there are health benefits to be derived from waiting until after puberty to spay or neuter your

dog.

However, there are also significant risks associated with owning an intact, maturing pet.

How seriously you take your responsibility as a pet owner is the biggest determining factor in

how risky it is to leave your dog intact until he or she matures. If you are responsible enough

to absolutely guarantee your unsterilized pet will not have the opportunity to mate, I would en-

courage you to wait until your pet is past puberty to spay or neuter.

If you are unable to absolutely guarantee you can prevent your dog from mating and adding

to the shameful, tragic problem of pet overpopulation, then I strongly encourage you to get your

animal sterilized as soon as it's safe to do so.

Please note: I'm not advocating pet owners keep their dogs intact indefinitely (see below). I'm also

not suggesting that shelters and rescues stop sterilizing young animals before re-homing them.

Shelter organizations can't determine how responsible adoptive pet owners will be. In this situation,

the risk of leaving adoptable animals intact is simply unacceptable. Shelters and rescues must im-

mediately spay/neuter pets coming into their care.

If you've adopted or rescued a dog sterilized at an early age, I encourage you to talk with

your holistic veterinarian about any concerns you have for your pet's future well-being, and what

steps you can take now to optimize her health throughout her life.

There is no one perfect answer to the spay/neuter question that fits every pet, and each situation

should be handled individually.

For Responsible Pet Owners, Decisions About When to Spay or Neuter Should be

Part of a Holistic Approach to Your Pet's Health and Quality of Life

If you own an intact pet, I can offer a general guideline for timing a spay/neuter procedure.

Your dog should be old enough to be a balanced individual both physically and mentally. This bal-

ance isn't achieved until a dog has reached at least one year of age. Although some breeds reach

maturity faster than others, many giant breed dogs are still developing at two years of age.

Other considerations include your dog's diet, level of exercise, behavioral habits, previous physical

or emotional trauma, existing health concerns, and overall lifestyle.

If you own an intact animal and need to make a spay/neuter decision, I encourage you to first learn

all you can about surgical sterilization options and the risks and benefits associated with the proce-

dures.

Talk with reputable breeders and other experienced dog owners, and consult a holistic vet to under-

stand what steps you can take to ensure the overall health and longevity of your pet.

Return to Karens Korner

10

REVIEW OF SEIZURES/EPILEPSY IN ANIMALS Dr. Jean Dodd’s Resource Blog

Seizures are the most common neurological disorder in dogs (Wong, 2013). Witnessing a beloved dog in the throes of a sei-

zure is terrifying; the fear that he will injure himself, that he shouldn’t be left alone or that his quality of life will suffer so much

that you will be forced to make a dire decision regarding his future are all enough to cause feelings of helplessness and con-

stant stress in even the most resilient dog parent. But the good news is that seizures do not necessarily get worse over time,

and there are proactive steps that can help reduce both their intensity and frequency (Canine Epilepsy Guardian Angels,

2011).

Minimizing the total number of seizures and decreasing their frequency is critical, since it’s theorized that every time the brain

has a seizure, it “learns” how to have the next seizure. This phenomenon is called “kindling,” and essentially it means that the

more seizures a dog has, the more likely he will continue to have them. It is a vicious cycle that becomes harder to break with

each episode (Canine Epilepsy Guardian Angels, 2011).

Seizures result from abnormal bursts of electrical activity in the brain. There are three main types:

Extracranial, which are caused by outside factors that affect the brain, such as a poison or low blood sugar. Diagnosis is

made via blood and urine tests.

Intracranial, or structural, result when there is something wrong inside of the brain, such as a brain tumor. These are more

worrisome and are diagnosed via MRI and spinal tap.

Idiopathic, which are the most common type, result from a functional problem in the brain in which the neurons over-fire,

causing the brain to become excessively excitable. Idiopathic seizures typically appear in dogs between one and five years of

age and most commonly affect Cocker Spaniels, Labrador Retrievers and German Shepherds, although any breed can suffer

from them (Wong, 2013).

Specific causes of seizures include:

Brain tumors

Certain medications

Environmental toxins

Fever

Food toxins

Hypoxia (inadequate levels of oxygen in the blood or tissues)

Infection

Inflammation

Inherited structural problems in the skull or brain (e.g., Syringomyelia, where a cyst forms in the spinal cord, damaging the

spinal cord and injuring nerve fibers that carry information from the brain to the extremities. This is especially prevalent in Cav-

alier King Charles Spaniels.)

Liver problems

Low blood sugar

Meningitis

Metabolic diseases (e.g., diabetes mellitus, thyroid disease)

Parasites

11

Sinus or ear infections

Strokes or clots

Stress

Systemic diseases (e.g., kidney or liver failure)

Tick-borne diseases

Traumatic injuries

Vaccinosis (adverse effects of vaccines)

Viruses (e.g., distemper, rabies)

(Canine Epilepsy Guardian Angels, 2011; Wong, 2013)

Be aware of the following signs that indicate the dog is having a seizure:

Falling over onto side

“Star gazing” or “fly snapping”

Convulsions

Loss of consciousness

Salivation

Stiffening and paddling motion of the legs

Uncontrolled urination and/or defecation

Vocalization

While one usually cannot stop a seizure once it’s started, steps to help reduce the severity and frequency include the following

listed below.

Eliminate Environmental Toxins and Other Exposures

Resistance to all disease involves an optimally functioning immune system, which can be damaged by environmental and food

toxins. Many other types of toxins have been linked to neurological issues.

Certain flea and tick treatments are unsuitable for dogs with seizures. The topical spot-on flea and tick control products

continue to raise concerns about their safety. In particular, products containing organophosphates and carbamates pose se-

vere health risks and should not be used on pets. Organophosphates are neurotoxins that kill insects by interfering with the

transmission of nerve signals in their brains and nervous systems. Like organophosphates, carbamates are toxic to the brain

and nervous system. If the product label lists atropine as an antidote to poisoning, the product most likely contains carbamates.

Spot-on flea and tick products containing pyrethroids have gained popularity over the last decade, as they are considered to be

less acutely toxic to birds and mammals than organophosphates and carbamates. However, these insecticides carry their own

potential toxicity risks. Pyrethrins are botanical insecticides derived from certain species of chrysanthemums. They work by

penetrating the nerve system and causing paralysis and eventual death of the target pests and have been linked with dizzi-

ness, headache, nausea, muscle twitching, reduced energy, changes in awareness, convulsions, loss of consciousness, hy-

perexcitability, tremors, profuse salivation and seizures in companion animals. Other flea and tick control products that are con-

traindicated for dogs prone to seizures are those containing spinosad (Comfortis®, Trifexis®), afoxolaner (NexGard™), or flu-

ralaner (Bravecto™).

Vaccines are linked to seizures. Distemper, parvovirus, rabies and, presumably, other vaccines have been linked with poly-

neuropathy, a nerve disease that involves inflammation of several nerves. Symptoms of polyneuropathy include muscular atro-

phy (wasting away of the muscle), the inhibition or interruption of neuronal control of tissue and organ function, muscular exci-

tation (stimulation of muscle fibers), incoordination (poor muscle control or coordination), weakness, and seizures. In addition,

12

MLV (modified live virus) vaccines are associated with the development of temporary seizures in both puppies and adult dogs

that belong to susceptible breeds or crossbreeds (Dodds, 2001).

Check Thyroid Function

Low thyroid function, known as hypothyroidism, can precipitate or aggravate existing seizure disorders. While the exact mecha-

nism of how this works is unknown, it may relate to the important role thyroid hormones play in cellular metabolism of the cen-

tral nervous system. In some cases, simply giving a hypothyroid dog the appropriate levels of thyroid medication reduces the

severity and frequency of the seizures, and may even stop them altogether. If a dog has seizures, it’s important that he has a

full thyroid antibody test profile run including Total T4, Free T4, Total T3, Free T3, and Canine Thyroglobulin Autoantibody

(TgAA). T3 Autoantibody (T3AA) and T4 Autoantibody (T4AA) can also be added. Since many veterinarians do not fully under-

stand how to properly test for canine thyroid dysfunction, the condition often goes undiagnosed or misdiagnosed, and the dog

unfortunately suffers unnecessarily. For this reason, it’s critical to carry out the testing at a lab specializing in interpreting thy-

roid dysfunction in dogs, such as Hemolife’s diagnostics lab. For more information on canine thyroid disorders, the most com-

mon endocrine dysfunction in dogs, please refer to our book, The Canine Thyroid Epidemic, DogWise Publishing, 2011.

Avoid Certain Dietary Ingredients

Dogs prone to seizures should not eat the following:

Foods that promote inflammation. Inflammation affects every organ in the body, including the brain, so it probably comes as

no surprise that inflammation can cause seizures. Dogs prone to seizures should not consume any potentially inflammatory

ingredients, including foods that trigger allergies or intolerances/sensitivities, such as chemical additives, wheat, corn, soy, beef

or cow’s milk products—but remember that it can also include any food that causes a problem for an individual dog. For dogs

with seizures, we advise testing with NutriScan to identify any problematic food ingredients. In particular, never give products

containing gluten to dogs with seizures, since gluten is specifically linked with neurological disorders, including epilepsy, and

promotes autoimmune thyroiditis (Kresser, 2010; Hyman, 2013).

Foods that cause fluctuations in blood sugar. Sugars can disrupt the body’s equilibrium or homeostasis, possibly leading to

seizures (Wilson, 2013). Avoid giving seizure-prone dogs carbohydrates with a high glycemic index (GI), including honey, sug-

ars, white rice, wheat, corn, white potatoes, carrots, and peas.

Foods containing glutamate and aspartate. Glutamate and aspartate are two excitatory non-essential amino acids

(Stafstrom, 2004; Wilson, 2013). Foods high in these amino acids include: grains, especially wheat, barley and oats; all cow’s

milk products (opt instead for goat’s milk, which is much lower); beans, especially soy, pinto, lima, black, navy and lentils; nuts,

especially peanuts, cashews and pistachios; seeds, including sunflower and pumpkin; any food sweetened with aspartame,

such as NutraSweet and Equal; rabbit; turkey; and monosodium glutamate (MSG), a glutamine salt. MSG is used in many pre-

pared foods and can appear on pet food labels under a number of pseudonyms, including “hydrolyzed vegetable protein”, “soy

protein extract” and “textured vegetable protein” (Wilson, 2013). These foods should also be avoided in dogs with liver dis-

ease.

Rosemary and oregano. Rosemary is commonly added as an antioxidant and anti-inflammatory to commercial pet foods.

While likely fine for most dogs, it is a neurotoxin that can promote seizures in vulnerable dogs. Oregano is also a powerful neu-

rotoxin and should not be fed to epileptics.

Vitamin/mineral deficiencies and seizures. Many vitamins and minerals are important for normal functioning of the nervous

system. Deficiencies in the minerals calcium, magnesium and sodium, for example, can affect electrical activity of brain cells

and result in seizures (Schachter, 2006). Calcium and magnesium, as well as zinc, are also referred to as sedative minerals

because they are calming for the nervous system (Wilson, 2013). Antioxidant vitamins (A, C and E) help boost the immune

system and fight inflammation. Perhaps the most important vitamins to protect against seizures are the B vitamins.

13

DNA Methylation: an Explanation for the “Kindling” Effect?

Kindling is a phenomenon whereby the more seizures an individual has, the more he will tend to have. Recently, scientists

have uncovered a possible reason for this phenomenon; which, not surprisingly, lies within the purview of epigenetics. Epige-

netics affects how DNA methylation impacts upon gene expression; and scientists are now recognizing that DNA methylation

also regulates processes that lead to neurologic disorders. A recent “methylation hypothesis” suggests that seizures them-

selves induce epigenetic modification of chromatin (the combination of DNA and proteins that make up the contents of a cell’s

nucleus) in a manner that aggravates an existing epileptic condition (Kobow, 2011). This means that, quite literally, seizures

“teach” cells how to have more seizures and that we can and need to interrupt this genomic “lesson” by reducing the frequency

of attacks. This hypothesis certainly provides a plausible explanation for the kindling effect, since everything that happens in

the body originates at the cellular level.

Since vitamin B-12 and folate promote optimum functioning of the DNA methylation cycle, deficiencies can lead to seizures.

Deficiency in biotin, another B-vitamin that modulates chromatin regulation, can also cause epilepsy. In people, a rare inherited

form of seizures known as pyridoxine-dependent epilepsy results from mutations in the ALDH7A1 gene, which leads to impair-

ment of normal vitamin B-6 function. Pyridoxine is involved in the breakdown of amino acids and the production neurotransmit-

ters, chemicals that transmit signals in the brain. Pyridoxine-dependent epilepsy does not respond to traditional medical thera-

py and is treated with high daily doses of pyroxidine (National Library of Medicine, 2013).

Thus, consuming a diet rich in B vitamins may help lower the susceptibility to seizures through their epigenetic ability to regu-

late gene expression (Foti & Roskams, 2011).

Omega-3 Fatty Acids: Too Important to Ignore

Research on the effects of omega-3 fatty acids and epilepsy are still in the early stages, however, we believe that this im-

portant nutrient makes perfect sense to help combat seizures. Omega-3s contain potent anti-inflammatory properties, and in-

flammatory mediators are increased in epileptic patients. Omega-3s also increase seizure thresholds, promote optimal brain

development and modulate neuronal excitability (Stafstrom, 2004; Yuen et al., 2005).

Ketogenic Diet: Proven Effective for People, but not for Dogs

A ketogenic diet contains high amounts of fat, low carbohydrates and moderate protein. Under normal circumstances, glucose

broken down from carbohydrates is the primary form of dietary energy. By severely limiting carbohydrates (and thus glucose),

the ketogenic diet mimics a constant state of starvation, forcing the body to burn fat for energy. The diet gets its name because

the fat is converted to ketones that are utilized as energy in place of carbohydrates. Ketogenic diets are often used in people

who do not respond to seizure medications, especially children. While it’s uncertain why they work, about two-thirds of people

on a ketogenic diet show significant improvement. But the diet can cause serious health problems, including GI tract upset,

hyperlipidemia, renal calculi, stunted growth and pancreatitis (Carr, 2013).

Ketogenic diets have never been proven effective, or safe, in dogs (Thomas, 2011.) In a 2005 study, researchers compared

the effects of a ketogenic diet containing 57% crude fat, 5.8% NFE (carbohydrates) and 28% crude protein to a control diet

containing 16% crude fat, 25% crude protein and 54% NFE (carbohydrates) in dogs diagnosed with idiopathic seizures. The

objective of the study was to determine if the ketogenic diet resulted in a significant reduction in seizure frequency. The dogs

were all receiving phenobarbital and/or potassium bromide and had experienced at least three seizures in the three months

prior to the study. All of the dogs were fed the control diet for a monitoring period of three to six months while their seizure fre-

quency was established. Dogs that had suffered five or more seizures during that time were randomly divided into two groups;

one group continued to receive the control diet, while the other group received the ketogenic diet. The dogs were evaluated at

14

0, 0.5, three and six months. Of the 12 dogs that completed the trial, there was no difference in seizure frequency between the

group fed the ketogenic diet and the control diet (Carr, 2013; Coates, 2013).

The fact that dogs can naturally tolerate longer periods without eating likely accounts for their lack of response to the ketogenic

diet. A high fat/low carbohydrate diet apparently just does not create the same biochemical changes in canines as it does in

people (Coates, 2013). Moreover, ketogenic diets may create adverse health effects in dogs. Pancreatitis is a serious condition

that often results from an excess of dietary fat. Due to a lack of proven efficacy and safety, we do not recommend a ketogenic

diet for dogs with seizures.

Could Seizures Originate in the Gut?

The importance of maintaining gut health and the role played by a compromised gastrointestinal (GI) system in leading to a

whole host of medical conditions cannot be overstated. Further, imbalances in intestinal microbial flora can also produce sei-

zures. The condition is known as “abdominal epilepsy” and it occurs due to the gut-brain connection. Abdominal epilepsy oc-

curs when an unhealthy microbial environment in the gut creates toxins that cross into the brain. In addition, sections of the

intestine known as Peyer’s Patches, where the gut connects with the lymphatic system, are closely associated with nerve bun-

dles and fibers directly connected with the brain, so intestinal irritation may result in seizures via this pathway. Many veterinari-

ans misdiagnose and so do not treat this type of seizure because rather than looking in the gut, they only look at the patient

“from the neck up.” If a dog suffers from seizures in combination with ulcerative colitis, manic itching or GI trouble (e.g., consti-

pation and/or diarrhea) he may have abdominal epilepsy.

Gelatin: Friend to the Dog Brain

Gelatin, a potent anti-inflammatory and brain protective food, is an important supplement for dogs with epilepsy (as well as for

arthritis and hip dysplasia). The primary amino acid in gelatin is glycine, which is known to protect against seizures and brain

damage (Canine Epilepsy Guardian Angels, 2011). Plain, unflavored gelatin can be added to the diet in many ways, such as

sprinkling it on the dog’s food or making treats out of it. However, never use Jell-O or other gelatins intended for dessert, as

they contain sweeteners (either sugar or artificial) that can potentially worsen the seizure condition (remember that the artificial

sweetener, Xylitol, is toxic to dogs).

Suggested Dose: (give twice a day, added to food)

10 to 25 lbs: 1 tsp (teaspoons)

25 to 50 lbs: 3 tsp

50 to 75 lbs: 6 tsp

75 to 100 or more: 3 tablespoons

Joanne’s Gelatin Dog Treats

This simple recipe for gelatin treats is provided courtesy of the late Joanne Carson, PhD, Founder of The Epi Guardian Angels.

They are like Gummy Bears for dogs!

Ingredients:

1 cup of unflavored gelatin

1 cup of cold, flavored liquid (such as broth)

1 cup of boiling liquid (either water or broth)

Put 1 cup of gelatin in a 1-quart bowl. Add 1 cup of the cold liquid and let stand one minute to soften. Pour 1 cup of boiling liq-

uid (water or broth) over the softened gelatin, and stir until the gelatin completely dissolves (about five minutes or less). For

chewier treats, add more gelatin. Pour the mixture into a 9 x 12 inch pan and let harden. Cut into 1 by 3 inch strips or an appro-

priate size for the dog.

15

It’s estimated that 20% of dogs on phenobarbitol anti-seizure medication develop liver enzyme induction (Canine Epilepsy

Guardian Angels, 2011). Liver cleansing herbs such as milk thistle and/or SAMe can be helpful.

Case Study Success!

Coal and corn do not mix.

Coal, a two-year-old female black Labrador Retriever, experienced seizures every other month. Hoping to avoid treating her

with anti-seizure medication, Coal’s guardians weaned her over to a prepared raw diet with lamb as the meat source. After dis-

cussing the options, an anti-inflammatory diet was chosen as the primary treatment. Coal was also treated with Western herbs

(lime blossom, valerian and chamomile) as well as coconut oil. The seizures stopped. Six months later, however, Coal experi-

enced another seizure after finding some taco shells in the garbage (made from corn). She had yet another seizure one month

later, which her guardians attributed to eating leftover popcorn from a slumber party. Three months later, Coal had another

seizure and her guardians remembered that she had licked several plates clean after a dinner that included corn-battered meat

and frozen corn. Over the next four years, Coal had only three seizures — all of which were connected to an episode of eating

corn! Thankfully, she never required anti-seizure medication.

* Adapted from: Dodds, WJ, Laverdure, D R. (2015) Canine Nutrigenomics: The New Science of Feeding Your Dog for Opti-

mum Health, Chapter 11; DogWise Publishing, Wenatchee, WA.

W. Jean Dodds, DVM

Hemopet / NutriScan

11561 Salinaz Avenue

Garden Grove, CA 92843

Return to Karens Korner

Penn/Baylor Med study describes underlying cause of di-

abetes in dogs

In a new effort, researchers from the University of Pennsylvania and Baylor College of Medicine have

used advanced imaging technology to fill in details about the underlying cause of canine diabetes, which

until now has been little understood. For the first time, they've precisely quantified the dramatic loss of

insulin-producing beta cells in dogs with the disease and compared it to the loss observed in people

with type I diabetes.

"The architecture of the canine pancreas has never been studied in the detail that we have done in this

paper," said Rebecka Hess, professor of internal medicine at Penn's School of Veterinary Medicine and

a study author.

Despite important differences between the disease in dogs and humans, the study also identified key

similarities that suggest investigating diabetes in dogs may yield valuable insights into treating humans.

16

The research was led by Emily Shields, currently a graduate student in Penn's Perelman School of Medi-

cine, who completed much of the work as a high school and then college student in labs at Penn and

Baylor. Jake A. Kushner, formerly of Penn and now McNair Medical Institute Scholar and chief of pediat-

ric diabetes and endocrinology at Baylor College of Medicine, was senior author. Together with Hess,

they collaborated with Penn Vet's Thomas J. Van Winkle, Matthew M. Rankin of Penn Medicine and Chil-

dren's Hospital of Philadelphia and Baylor's Carol J. Lam and Aaron R. Cox.

Their study was published in PLOS ONE.

Canine diabetes can be managed with insulin, similar to type I diabetes in humans. But, unlike the hu-

man version of the disease, dogs typically develop diabetes in middle or old age, while people with type

1 diabetes are typically diagnosed during childhood. In addition, while type 1 diabetes is known to be an

autoimmune condition, researchers haven't found conclusive evidence that the same is true in dogs.

To learn more about the factors that contribute to canine diabetes, the researchers made use of a reposi-

tory of donated tissue samples from dogs -- 23 with diabetes and 17 without -- who had been treated at

Penn Vet's Ryan Hospital and later died.

The team used robotic microscopes that can rapidly move around a slide taking images of pancreas tis-

sue samples, which were analyzed by computer to determine the contents.

"In a larger view we could look at the entire cross-section of pancreas to determine how many islets

there were and how big they were," Shields said. "Then we could zoom in to differentiate beta cells,

which produce insulin, from alpha cells, which produce glucagon."

They found that beta cells dropped off in dramatic fashion in diabetic dogs, reduced 13-fold compared to

non-diabetic animals. They also found that non-diabetic canine islets contained a large percentage of

beta cells, comprising about 80 percent of endocrine cells. In contrast, beta cells comprise slightly more

than 50 percent of endocrine cells in non-diabetic human islets. The researchers noted that this may

mean that dogs need to lose more beta cells before experiencing symptoms of diabetes. The observa-

tion could explain why dogs develop a form of diabetes that is similar to type 1 diabetes, but do so later

in life, compared to humans.

They also identified features of the islets and pancreatic structures that were different in dogs than in hu-

mans.

"In sharp contrast to human diabetes, in which there are a lot of islets still present but none contains in-

sulin, we found in dogs that only a few beta cells were present and the islets were incredibly small,"

Kushner said.

17

While the researchers had hoped to be able to visualize immune cells infiltrating the pancreas and at-

tacking beta cells, they failed to do so. While other signs point to canine diabetes being an autoimmune

condition, this study did not find a "smoking gun."

Though the work highlights differences between canine and human diabetes, it also points to a number

of similarities that distinguish the two from diabetes in rodents, which are often used as models to study

the disease.

For example, the scientists observed that dogs' beta cells were distributed throughout the islets, as beta

cells in humans are. In rodents, beta cells are concentrated in the center of the islet.

"Now that we know more about the disease in dogs and in particular how they are similar to humans in

ways that rodents are not, it makes them more appealing as a model," Kushner said.

At Penn, Hess is currently working to look for genetic markers in dogs that heighten a dog's risk of devel-

oping diabetes.

"My hope is that with genetic screening we can eventually identify pre-clinical diabetic dogs, potentially

making breeding recommendations that could decrease the incidence and prevalence of the disease in

dogs," Hess said.

Adapted by MNT from original media release

Return to Karens Korner

Penn/Baylor Med study describes underlying cause of di-

abetes in dogs

In a new effort, researchers from the University of Pennsylvania and Baylor College of Medicine have

used advanced imaging technology to fill in details about the underlying cause of canine diabetes, which

until now has been little understood. For the first time, they've precisely quantified the dramatic loss of

insulin-producing beta cells in dogs with the disease and compared it to the loss observed in people

with type I diabetes.

"The architecture of the canine pancreas has never been studied in the detail that we have done in this

paper," said Rebecka Hess, professor of internal medicine at Penn's School of Veterinary Medicine and

a study author.

Despite important differences between the disease in dogs and humans, the study also identified key

similarities that suggest investigating diabetes in dogs may yield valuable insights into treating humans.

18

The research was led by Emily Shields, currently a graduate student in Penn's Perelman School of Medi-

cine, who completed much of the work as a high school and then college student in labs at Penn and

Baylor. Jake A. Kushner, formerly of Penn and now McNair Medical Institute Scholar and chief of pediat-

ric diabetes and endocrinology at Baylor College of Medicine, was senior author. Together with Hess,

they collaborated with Penn Vet's Thomas J. Van Winkle, Matthew M. Rankin of Penn Medicine and Chil-

dren's Hospital of Philadelphia and Baylor's Carol J. Lam and Aaron R. Cox.

Their study was published in PLOS ONE.

Canine diabetes can be managed with insulin, similar to type I diabetes in humans. But, unlike the hu-

man version of the disease, dogs typically develop diabetes in middle or old age, while people with type

1 diabetes are typically diagnosed during childhood. In addition, while type 1 diabetes is known to be an

autoimmune condition, researchers haven't found conclusive evidence that the same is true in dogs.

To learn more about the factors that contribute to canine diabetes, the researchers made use of a reposi-

tory of donated tissue samples from dogs -- 23 with diabetes and 17 without -- who had been treated at

Penn Vet's Ryan Hospital and later died.

The team used robotic microscopes that can rapidly move around a slide taking images of pancreas tis-

sue samples, which were analyzed by computer to determine the contents.

"In a larger view we could look at the entire cross-section of pancreas to determine how many islets

there were and how big they were," Shields said. "Then we could zoom in to differentiate beta cells,

which produce insulin, from alpha cells, which produce glucagon."

They found that beta cells dropped off in dramatic fashion in diabetic dogs, reduced 13-fold compared to

non-diabetic animals. They also found that non-diabetic canine islets contained a large percentage of

beta cells, comprising about 80 percent of endocrine cells. In contrast, beta cells comprise slightly more

than 50 percent of endocrine cells in non-diabetic human islets. The researchers noted that this may

mean that dogs need to lose more beta cells before experiencing symptoms of diabetes. The observa-

tion could explain why dogs develop a form of diabetes that is similar to type 1 diabetes, but do so later

in life, compared to humans.

They also identified features of the islets and pancreatic structures that were different in dogs than in hu-

mans.

"In sharp contrast to human diabetes, in which there are a lot of islets still present but none contains in-

sulin, we found in dogs that only a few beta cells were present and the islets were incredibly small,"

Kushner said.

19

While the researchers had hoped to be able to visualize immune cells infiltrating the pancreas and at-

tacking beta cells, they failed to do so. While other signs point to canine diabetes being an autoimmune

condition, this study did not find a "smoking gun."

Though the work highlights differences between canine and human diabetes, it also points to a number

of similarities that distinguish the two from diabetes in rodents, which are often used as models to study

the disease.

For example, the scientists observed that dogs' beta cells were distributed throughout the islets, as beta

cells in humans are. In rodents, beta cells are concentrated in the center of the islet.

"Now that we know more about the disease in dogs and in particular how they are similar to humans in

ways that rodents are not, it makes them more appealing as a model," Kushner said.

At Penn, Hess is currently working to look for genetic markers in dogs that heighten a dog's risk of devel-

oping diabetes.

"My hope is that with genetic screening we can eventually identify pre-clinical diabetic dogs, potentially

making breeding recommendations that could decrease the incidence and prevalence of the disease in

dogs," Hess said.

Adapted by MNT from original media release

Return to Karens Korner

Spay, neuter, or shot? How an injection could be the fu-

ture of animal control

A single shot into the muscle is enough to stop egg and sperm production in mice, report California Insti-

tute of Technology scientists on October 5 in Current Biology. The injection delivers packaged DNA into

muscle cells, causing them to produce neutralizing antibodies against male and female reproductive hor-

mones. All mice that received the shot were unable to sire offspring after about two months, with no side

effects. The researchers see this proof-of-concept study as the first step for developing a cheap alterna-

tive to spaying or neutering feral animals.

"The field of immunocontraception has been around for many, many decades but has always run up

against the variability in the immune response," says senior study author Bruce Hay of Caltech. "In re-

20

cent years, a number of labs have shown that you can express high levels of antibodies in small and

larger animals to prevent disease. We thought: why not try it to manipulate physiology as well?"

Hay wanted to experiment with an antibody that could neutralize gonadotropin-releasing hormone

(GnRH) in mice. GnRH is made in the brain and acts on the pituitary gland to promote the secretion of

reproductive hormones that stimulate egg and sperm development--so it is an ideal target to render an

animal infertile.

His lab, led by first author Juan Li, then took the gene for an anti-GnRH antibody and packaged it inside

the shell of an adeno-associated virus (a virus type that commonly infects mammals but causes no

symptoms). Once injected inside the muscle, the DNA is unpackaged and handed over to the muscle

cells, which use it to become antibody factories. Unlike immune cells, muscle cells rarely turn over, so

they can produce the antibodies for an animal's lifetime. (Other studies have shown that production of

protein continues for at least 10 years, but no study has looked at how long this ultimately lasts.)

In addition to using an anti-GnRH antibody, Hay's lab also blocked fertility in female mice using an anti-

body that binds a protein layer called the zona pellucida, which surrounds egg cells. This antibody blocks

sperm binding without affecting female hormonal cycling.

"Spaying and neutering wild animals is not a trivial process--it takes money and time to anesthetize

them, do the surgery, and let them recover," Hay says. "This is a much more benign way of managing

populations."

Could the shot work for humans? Not right now, and not in the same way. Anti-sperm antibodies are pre-

sent in some infertile humans, but up until the recent development of gene-therapy-based approaches,

there's been no easy way of directly delivering the antibody in humans without regular injections.

"Therefore, it's now possible to give someone the antibody, in the form of a gene, and ask if it has con-

traceptive effects," Hay says. "It's a long road to develop any new drug, but it might someday provide an

alternative to current, surgical methods of permanent contraception."

Another hurdle is the lag time between injection and when an animal (or person) becomes fully infertile.

Hay predicts that other forms of gene delivery could yield a much more rapid onset, and it's an active ar-

ea of investigation.

In the meantime, his group is carrying out a pilot study on female cats in collaboration with Bill Swanson,

Director of Animal Research at the Cincinnati Zoo's Center for Conservation and Research of Endan-

gered Wildlife, with the goal of managing local populations.

Return to Karens Korner