Loves Delta Breeze Farm

09/21/2025

If you try to negotiate a circle or corner without bending your horse, then your horse’s body will remain straight, and he will need to lean inwards in order to make the turn.

Leaning around circles, corners, and turns presents several problems.

❌ Your horse will overly stress his joints and ligaments on the inside, which can cause strain and/or injury. (Remember that when being ridden, your horse is also carrying the added weight of his tack and you.)
❌ Your horse will be unable to engage his hind legs underneath him and will, therefore, be on his forehand.
❌ True collection will not be possible, again, because your horse cannot engage his hind legs.
❌ Your horse will find smaller circles and tighter turns difficult.
❌ Your horse will be unable to work through to the contact.
❌ Your horse will be unable to perform and be positioned for lateral movements, such as shoulder-in, travers, and half-pass.
❌ More than likely, the tempo will be rushed and inconsistent.
❌ It will make the dressage arena feel much smaller and more difficult to negotiate.
❌ In extreme cases, especially if you are riding on slippery or uneven ground, your horse can fall over onto his side.

Furthermore, this isn’t just a problem for the discipline of dressage. If you go showjumping, being unable to bend your horse will make him unbalanced around turns, and he will most likely fall inwards through the corners of the arena, leaving you with less space to prepare for the next fence and less chance for your horse to see it. This can result in a pole down, a stop, or a runout.

The big point is that you do not want your horse to lean around corners. Instead, you want your horse to stay upright, and your horse can only stay upright if you ask him to bend correctly.

Stock image from Shutterstock.

Link in description for how to bend your horse correctly 👇

09/09/2025

Shivers in Horses
Brian S. Burks, DVM
Diplomate, ABVP
Board Certified in Equine Practice

Shivers is a chronic progressive neuromuscular disease of unknown etiology. It is characterized by involuntary muscle tremors, spasms, and cramping, primarily affecting the hind limbs, tail, and sometimes the head and neck. Occasionally, there is generalized hypertonia and the thoracic limbs are affected. The disease is most common in draft horses, including Belgians, Percherons, Clydesdales, shires, Haflingers, Norwegian Fjord, Suffolk, Irish Draft, Draft crosses, and Draft Mule, but other breeds (Warmbloods, light horses) may be affected. While shivers can affect horses of any s*x, geldings are three times more likely to be diagnosed with the disorder than mares. Horses taller than 16.3 hands are also more susceptible than shorter horses. The majority of horses show signs before the age of five years.

The etiology of shivers is unknown, but there is damage to specialized nerve cells (Purkinje cells) of a specific area of the cerebellum. The cerebellum regulates slow, learned movements, such as backing. Forward, faster gaits are regulated by separate spinal circuits, allowing affected horses to compete, even at high levels. Horses with shivers lack the “off-switch” the cerebellum normally provides for muscle contraction, causing the muscles to be constantly active. This may be a genetic disorder.

Shivers should be distinguished from several diseases:
Stringhalt results in more flexion and occurs when moving forward. Stringhalt has a spasmodic and excessively rapid flexion of one or both hind-limbs. The hocks are flexed violently and suddenly toward the abdomen and are brought forcibly to the ground in one quick movement. Severely, and bilaterally, affected horses have a ‘bunny hopping’ gait. Most strides are abnormal.
Fibrotic myopathy results from scar tissue formation following injury to the semitendinosus and semimembranosus muscles. The gait is usually characterized by an abnormal slapping-type hind-limb gait with a lower arc of the limbs than seen with shivers or stringhalt. Horses with fibrotic myopathy can back normally. Adult Quarter horses are the most frequently affected breed.
Stiff horse syndrome is characterized by intermittent stiffness and spasms in the back and pelvic limb muscles. There is muscular hypertrophy. The movements become more normal when walking more than a few steps, or during trotting. In people, stiff person syndrome is an immune-mediated deficiency of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter of the central nervous system.

Clinical signs of Shivers can be difficult to detect in mildly affected individuals, and because signs occur at irregular intervals. Affected horses show signs when being asked to back or turn, or when forced to step over an object. The affected limb will be partially flexed and abducted (held away from the body). The muscles of the upper limb and tail may tremor. They may stand base-wide or base-narrow instead of an even stance. Affected horses may exhibit hyperextension (feet are placed further back than normal) of the hind limbs when backing up. In a few cases, muscles of the face and neck may contract spasmodically. In severe cases, clinical signs are observed when the horse moves forward, usually only for a few steps or when turning sharply. Muscle atrophy, especially of the thigh muscles, occurs as the disease progresses. This often leads to hindquarter weakness. Clinical signs usually resolve in a short time, and the horse will appear clinically normal when standing still or trotting, with signs reappearing when the horse is asked to turn or back.

There are two primary categories of Shivers signs observed while backing:
• Hyperflexion: One hindlimb is raised up and away from the body in a spastic state for several seconds to several minutes. The limb trembles or “shivers” in suspension, then the foot is brought rapidly to the ground when the spasms subside. One or both hind-limbs may be affected.
• Hyperextension: The horse places the hind feet further back than normal when moving backwards with the stifle and hock joints hyperextended. Both forelimbs are also extended when backing begins, resulting in a stretched or “sawhorse” stance. In severe cases one or both hind limbs may be held out behind the animal in rigid spastic extension, resulting in instability and even falling if the horse cannot regain control of one leg to catch itself. The horse may stand on its toes with the heels raised off the ground. Most horses are affected in both hind limbs.

Horses with shivers are resistant to hind-limb flexion and may hyperflex the opposite hind leg before flexing and abducting the hind-limb being touched. These signs may occur when the hind feet are picked up to be cleaned or when the horse is being shod, especially when the foot is hammered during shoeing. The condition may progress so that the horse becomes impossible to shoe. Excitement, such as leading the horse from the stall, or when footing changes, may worsen clinical signs. Such horses improve when turned out on pasture. Offering a bucket of water on the ground can also stimulate clinical signs. As the neck is extended, muscle spasms occur in the hindquarters, with the front feet planted firmly. The body sways backward, the back is arched, and the tail is je**ed to an elevated position.

Occasionally the muscles of the forelimbs, neck, trunk and face may occur. The forefoot is thrust forward into extension, with the foot barely touching the ground. The extensor muscles above the elbow quiver. When facial muscles are involved, there is rapid blinking, quivering ears, and lip twitching. These signs are considered rare.

There is no specific diagnostic test for shivers. Diagnosis is based upon clinical signs and ruling out other diseases such as stringhalt, equine protozoal myeloencephalitis (EPM), and others through lameness and neurological examinations along with other diagnostic testing. It is important to recognize that many horses may demonstrate hyperflexion when asked to pick up their hind feet, but they back up normally. These horses do not have shivers but instead likely have an underlying orthopedic issue. A diagnosis of shivers requires the horse to demonstrate clinical signs while backing up.

There is no treatment for the disease other than consistent exercise and a low carbohydrate/high fat diet. Provision of vitamin E is may slow the progression, though it will not improve the clinical signs of shivers. The disease is slowly progressive and the prognosis for affected horses is poor.

Veterinary evaluation of horses with suspected shivers is essential. A thorough lameness exam can rule out other causes of lameness or other abnormalities. The exam should have horses back and the limb should be flexed.

Fox Run Equine Center

www.foxrunequine.com

(724) 727-3481

09/09/2025

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09/02/2025

Vitamin E in Horses
Brian S. Burks, DVM
Diplomate, ABVP
Board-Certified in Equine Practice

Vitamin E is a fat-soluble vitamin that acts as a biological antioxidant, in conjunction with selenium and vitamin C, protecting the body from oxidative stress of exercise, illness, and certain medical conditions. It maintains neuromuscular function and positively affects the immune system. It enhances both humoral and cell-mediated immunity. It aids in utilization of vitamin K. Too much vitamin E decreases vitamin A absorption, and can even interfere with its function.

Vitamin E naturally exists in eight different forms (alpha-, beta-, gamma-, and delta-tocopherols and tocotrienols) each of which has slightly different activity in the body. Even though there are 8 forms of vitamin E, the most biologically active form of the vitamin is called alpha-tocopherol. Alpha-tocopherol is considered the most active natural form because it is the preferred form of vitamin E transported and used by the liver. It is an essential vitamin, meaning that it is not synthesized in the horse.

Natural vitamin E is found in lush, green pasture and is stored in the liver, and in fat, for use during the winter months. Natural vitamin E is found in some nutritional supplements. Vitamin E levels degrade rapidly during hay cutting and storage, making supplementation essential for horses not on fresh pasture, such as stall-kept, breeding, and performance horses. The most biologically active natural form is RRR-alpha-tocopherol, which is more readily absorbed than synthetic versions and is available in various supplement forms.

Natural vitamin E comes from plant oils instead of petroleum. Due to its molecular structure, natural vitamin E is much better absorbed in the body. Specific transport proteins in the liver tend to bind better to natural vitamin E, allowing it to be transported to other tissues in the body to be used for important functions, including as an antioxidant.

Low vitamin E level is a risk factor for neuromuscular diseases such as equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (eNAD/EDM), equine motor neuron disease (EMND), and vitamin E responsive myopathy. Such horses may have poor coordination, ataxia, muscle tremors, and weakness. Other clinical signs include a poor immune response, lack of muscle mass, slow recovery from exercise, and low energy or lethargy. Further, vitamin E deficient horses may have patchy, dry, and inflamed fur, skin, or mane.

The recommended daily amount of natural Vitamin E consumed by your horse is 1,000 international units (IU’s). Horses in heavy work will require more vitamin E. If your horse is diagnosed as deficient based on a blood sample, very high daily levels, up to 10,000 IU daily, are recommended to restore normal levels quickly. It often takes weeks to months after initiating supplementation to bring a deficient horse’s vitamin E levels back into the normal range. These high levels of Vitamin E are safe to supplement, but choosing the right supplement is also important.

To know if your horse is vitamin E deficient, a blood sample is needed to measure serum levels. If serum levels are low, then supplementation is required. When evaluating vitamin E in a product, there are two main types—natural and synthetic. The synthetic form of vitamin E is known as dl-alpha-tocopherol, and the natural form is d-alpha-tocopherol. Both forms work, but natural vitamin E is more readily absorbed and requires lower levels of supplementation.

Symptoms of excessive vitamin E include easy coagulopathy, impaired bone generalization, abdominal cramps, diarrhea, fatigue, and muscle weakness. High doses of vitamin E, typically from supplements, can interfere with blood clotting, increasing the risk of hemorrhages, including bleeding in the brain. These signs occur when supplementation exceeds 10,000 IU per day.

Vitamin E is an important fat-soluble, essential vitamin. Deficiency of this vitamin primarily results in neuromuscular dysfunction in the horse. Toxicity, although rare, is an important consideration when supplementing this vitamin. Caution should be used when used in combination with selenium.

Fox Run Equine Center

www.foxrunequine.com

(724) 727-3481

08/30/2025

Olympian Isabell Werth explains how elasticity and suppleness allow your dressage horse to do his job well and how to help him achieve these key qualities.

08/29/2025

08/29/2025

Excellent!

Endocrine-Associated Laminitis
Brian S. Burks, DVM
Diplomate, ABVP
Board-Certified Equine Specialist

Laminitis occurs when the laminae (leaves) that suspend the third phalanx within the hoof capsule become damaged and inflamed. Given enough damage, they separate, allowing the coffin bone to rotate or sink.

Laminitis is not only a local disease, it is also systemic. About 12% of laminitis cases are caused by colic, diarrhea, retained placenta, or carbohydrate overload. The remaining cases are related to diet, obesity, and/or endocrine disorders- equine metabolic syndrome and pituitary pars intermedia dysfunction (PPID)/equine Cushing’s disease.

Equine metabolic syndrome (EMS) typically causes horses to become obese, with regional adiposity and a cresty neck. They are predisposed to weight gain and refractory to weight loss. Not all EMS horses are obese; some high-risk breeds are thin, and weight loss is not always enough to prevent endocrine disease.

In the United States, 51% of mature light-breed horses are obese. Genetics contribute to body condition and altered endocrine function.

Adipocyte hypertrophy, inflammation and increased CCL2 (cytokine) expression are features of obese adipose tissue in horses but fibrosis and altered adipose tissue expression of insulin-signaling genes are not consistent features. Visceral and retroperitoneal adipose tissue of horses with obesity and EMS is markedly dysfunctional with a hypertrophic-inflammatory phenotype.

Evidence of increased cortisol levels over a prolonged period does exist; there is an abnormal fat pad distribution, elevated circulating insulin levels, glucose intolerance, laminitis, hyperlipemia with hepatic lipidosis, and infertility.

Laminitis is common in these horses due to circulating HSD, leading to elevated endogenous cortisol levels. Other risk factors for laminitis are lacking in these horses. The laminitis may be chronic and low grade, but acute exacerbations can occur. Corticosteroids lead to hyperinsulinemia, which has been shown to cause laminitis. Glucocorticoids enhance the vasoconstrictive effects of epinephrine, norepinephrine, and serotonin. Obese horses have altered blood flow due to endothelial dysfunction from insulin insensitivity and increased vasospasticity. There is also a hypercoagulable state similar to atherosclerosis in humans.
The nutrition and body condition of a pregnant mare could be another contributing factor to a foal’s endocrine state later in life.

Intestinal health may also play a role in that the microbiome of EMS horses is less diverse, similar to humans with metabolic syndrome. Human MS has been linked to loss of intestinal barrier function, increased intestinal permeability or leaky gut syndrome, which adds to systemic inflammation. This likely occurs in horses as well.

Endocrine-disrupting chemicals (EDCs) are also associated with EMS, with reports that they alter gene expression and affect metabolism. Many EDCs persist in fat for prolonged periods.

Dysfunction of the pituitary pars intermedia, usually in older horses, also causes laminitis. That portion of the pituitary hypertrophies, leading to excessive production of pituitary hormones, particularly adrenocorticotropin hormone (ACTH), which in turn amplifies cortisol (the stress hormone) secretion from the adrenal glands. Horses with PPID are hirsute, with long, shaggy coats that do not shed out well, and grow in faster in the autumn. They have abnormal fat distribution and undergo muscle wasting. They drink and urinate excessively and have recurrent infections, such as sinusitis, hoof abscesses, and poor wound healing. Affected horses may be infertile. Many also experience hyperinsulinemia, amplifying the risk of laminitis.

Insulin dysregulation is a consequence of obesity and is also found in many PPID horses, leading to laminitis. Dietary glucose absorbed into the bloodstream stimulates the pancreas to secrete insulin. With ID, cells do not respond to insulin signals to take glucose into muscle, liver, and fat cells. The pancreas then secretes increasing amounts of insulin in an attempt to increase glucose uptake. Normally, the liver clears most insulin, but horses with obesity or ID do not clear insulin as well.

Intestinal changes also contribute to hyperinsulinemia. There are specialized endocrine cells throughout the intestinal tract, along the mucosal surface, and their interaction with the microbiota increases secretion of incretin (stimulating a decrease in blood glucose levels) hormones such as glucagonlike peptides (GLP1 and 2) in response to high nonstructural carbohydrate (NSC) meals, like grain. GLPs are implicated in inducing more pronounced and undesirable insulin responses.

Insulin alters the signaling within the lamellar epithelial cells, causing them to change shape and stretch due to disruption of the cell cytoskeleton.

Endocrine-associated laminitis often begins with a long subclinical phase that causes chronic changes to the hoof capsule. The horse will develop divergent hoof rings that are wider at the heel than the toe that can go all the way down the hoof capsule, indicating that although the horse may not have clinical signs of laminitis, it has been present for at least one year. Others have more obvious signs, including flaring or distortion of the dorsal hoof wall, a flat or convex sole, and widening of the white line region. The horse may develop overt lameness without warning.

This differs from other forms of acute and chronic laminitis related to systemic inflammatory response syndrome (SIRS) that develops from colitis, endotoxemia, placentitis, or carbohydrate (grain) overload. In these cases, inflammatory cells infiltrate the laminae and the basement membrane that soon degenerates and the lamellae fail. This does not occur with endocrine induced laminitis, which is more nebulous.

Knowing that many cases of laminitis are attributable to endocrine disease, steps can be taken for prevention and treatment before lameness is severe. Growth rings in the hoof capsule can be present for many months without lameness, giving the opportunity to control insulin dysfunction and laminar stretching and failure with painful laminitis.

Controlling obesity is paramount to controlling insulin dysfunction and endocrinopathic laminitis. Refrain from overfeeding your horse, and restrict or eliminate pasture turnout during periods of high sugar accumulation in grass. Your veterinarian can help tailor a dietary program that provides sufficient and safe levels of nutrients compatible with your horse’s needs. Implement lifestyle changes that include not only dietary controls but also regular exercise for your horse.

Fox Run Equine Center

www.foxrunequine.com

(724) 727-3481

08/26/2025

Vitamins and Minerals
Brian S. Burks, DVM
Diplomate, ABVP
Board Certified in Equine Practice

Vitamins and minerals are part of six essential ingredients required by horses. The others are water, carbohydrates, protein and fat. Horses that are not in heavy work are able to obtain sufficient amounts of these nutrients on good quality pasture and hay (water excepted). Horses only need small amounts of vitamins and minerals, but their lack can have a major impact on your horse’s health.

Vitamins
Vitamins are organic nutrients obtained by the diet or supplementation. They cannot be synthesized by the body. They have a diverse range of function as enzyme co-factors, hormones, and anti-oxidants. Vitamins can be either fat or water soluble.

Fat soluble vitamins are able only to dissolve in fat, not water. The fat soluble vitamins are A, D, E, and K, and are absorbed from the intestinal tract in small fat droplets. They are stored in the body’s fat tissue and liver. Hypervitaminosis is possible with these vitamins, so feeding only the recommended amounts is important, as too much can be harmful. The liver can hold a store of fat soluble vitamins to last as much as six months.

Vitamin A is a group of unsaturated nutritional organic compounds that includes retinol, retinal, retinoic acid, and several provitamin A carotenoids. Vitamin A has multiple functions: it is important for reproduction, growth and development, for the maintenance of the immune system, healthy skin, and good vision. The precursor to vitamin A is present in fresh grass, but rapidly lost from hay. A horse’s vitamin A requirement is 30-60 IU/kg of body weight per day.

Vitamin D is a group of fat-soluble secosteroids responsible for increasing intestinal absorption of calcium, magnesium, and phosphate, and multiple other biological effects. The most important compounds in this group are vitamin D₃ and vitamin D₂. Vitamin D is present in grass, alfalfa, and grass hay. Vitamin D becomes a hormone when activated and is responsible bone formation. Horses require at least 6.6 IU/kg/day or 3300 IU/day. This is produced with about 6-8 hours of sunlight per day.

Vitamin K is a group of structurally similar, fat-soluble vitamins found in foods and in dietary supplements. The body requires vitamin K for complete synthesis of certain proteins that are needed for blood coagulation and for controlling binding of calcium in bones and other tissues.

Vitamin E is a group of eight fat soluble compounds that include four tocopherols and four tocotrienols. It is found in grass and hay, but it decreases in hay over time. Vitamin E deficiency, which is uncommon and usually due to an underlying problem with digesting dietary fat rather than from a diet low in vitamin E, can cause nerve problems. Vitamin E is an anti-oxidant important for nerve function and protection. Its deficiency has been linked to equine degenerative myelopathy and equine motor neuron disease, especially in horses not on pasture, which has plenty of vitamin E, as levels will decrease over time in hay. Healthy horses require about 1-2 IU/kg/day of vitamin E.

Water soluble vitamins include Vitamin C and B, and are not typically stored in the body, so that daily intake is important.

B vitamins are a class of water-soluble vitamins that play important roles in cell metabolism. Though these vitamins share similar names, they are chemically distinct compounds that often coexist in the same foods. In general, dietary supplements containing all eight are referred to as a vitamin B complex. B-vitamins have a variety of functions, helping to maintain healthy skin and muscle, promoting cell growth, and enhancing the immune and nervous systems. There are eight B vitamins. Vitamin B7 is biotin, important in maintaining foot health; horses need at least 20mg per day. These vitamins are generally found in good quality forages and are made by the bacteria in the equine hindgut. Vitamin B12 synthesis requires adequate amounts of cobalt in the diet.

Supplementation of B vitamins might be useful during disturbances of the microbial population in the colon which can occur due to high grain rations, stress, or other illness.

Vitamin C, also known as ascorbic acid and l-ascorbic acid, is a vitamin found in various foods and sold as a dietary supplement. Vitamin C is an essential nutrient involved in the repair of tissue and the enzymatic production of certain neurotransmitters. It is a potent antioxidant and is involved in a variety of enzyme systems and is required to synthesize collagen found in tendon and ligaments. Deficiencies of this vitamin are rare as it is synthesized in the hind gut from glucose. Supplementation may be necessary with disturbances of the microbial population in the horse’s colon.

Minerals are defined as elements or chemical compounds that are normally crystalline and formed by geologic processes. Minerals support biochemical processes of the body and serve both structural and functional roles.

Calcium and phosphorus are important minerals of bone. The Ca:P ratio for adult horses is 1:1 to 2.5:1; phosphorus should not exceed calcium intake. Idle mature horses require about 20grams of calcium per day; this can double for a horse in regular heavy exercise.

About 99% of calcium is found in bones and teeth. Bone is 35% calcium. Calcium is important for muscle contraction, cell membrane function, blood coagulation, and the regulation of many enzymes. Alterations in Ca:P can result in the condition known as “big head”, “bran disease”, or “Miller’s disease” where the bones do not form properly and are soft; pathologic fractures can result.

Hypocalcemia, or low blood calcium, can result in hypersensitivity of the phrenic nerve, which passes over the cardiac base to innervate the diaphragm. Each time the heart contracts, the diaphragm will contract, resulting in a condition known as synchronous diaphragmatic flutter or “thumps”.

Iron binds oxygen within red blood cells and transports the oxygen throughout the body for other cells to use. Sulfur is important for structural proteins like those of articular cartilage and connective tissues. Zinc is an important co-enzyme in many systems. Copper is a co-enzyme and is important in elastic tissues such as tendons. Selenium is an anti-oxidant that works in tandem with vitamin E, and is important for the immune and muscular systems.

Minerals also function as electrolytes, which are minerals with charged particles known as ions when dissolved in water. These include sodium, potassium, and chloride. They are important for muscle contraction and conducting nerve impulses. Electrolytes also control the flow of fluids in the body, holding fluids in the vascular system and cells in a controlled fashion.

Sodium is an essential electrolyte that helps maintain the balance of water in and around cells. It is important for proper muscle and nerve function. It also helps maintain stable blood pressure levels. Insufficient sodium in blood is also known as hyponatremia, while too much is hypernatremia. The NRC states that about 50grams (100mg/kg) of sodium is needed per day, though horses only voluntarily eat about 60mg/kg of salt per day.

Potassium is an electrolyte necessary for proper muscle function. Along with other electrolytes such as sodium and calcium, potassium plays an important role in normal muscle contraction and relaxation. Elevated concentrations of potassium, a condition known as hyperkalemia, can be life-threatening.

Forages contain large amounts of potassium, so supplementation is only necessary in horses that sweat large volumes. Horses are obligate potassium secretors and will require supplementation if not eating.

In healthy horses, the kidneys filter out excess potassium from circulation, which is then excreted in urine. When the kidneys fail to clear potassium, or when too much potassium moves from inside to outside of cells, hyperkalemia can result. Abnormally high concentration of potassium in the blood causes muscles to become weak and an irregular heartbeat. At a greater risk of hyperkalemia are horses with a history of hyperkalemic periodic paralysis (HYPP), compromised kidney function, or massive cellular destruction, such as after trauma, burns, or a severe episode of rhabdomyolysis (tying-up).

Classic signs of hyperkalemia include muscle weakness, trembling, depression, and lethargy. While these symptoms are general, when accompanied by changes in cardiac rhythm, hyperkalemia should be suspected. Cardiac changes are not always present in cases of hyperkalemia, so the absence of cardiac abnormalities should not rule out such a diagnosis.

A little bit is good, but too much can be harmful. Vitamins can be toxic. Too much mineral can interfere with absorption and metabolism of other minerals. When offering multiple supplements it is important to total the amounts to be sure not to exceed requirements. Too much supplementation is dangerous for the body and is not economical.

Fox Run Equine Center

www.foxrunequine.com

(724) 727-3481

08/24/2025

🐴DRESSAGE SOLUTIONS🐴 Improve Rein Connection

To improve your rein connection ...

Imagine your point of contact with the bit is in your elbows, triceps and back, and that your arms, wrists and hands are just extensions of the reins. This allows the connection to be held in your body rather than your hands and allows the hands and arms to be soft.
~ Jessica Miller

🎨 Sandy Rabinowitz

08/18/2025

Life is too short to be serious all of the time.

05/04/2025